@article{%a1.%Y_247,

title = {Farnesoid X Receptor Agonist INT-787 Inhibits Hepatic Mitochondrial Dysfunction in a Diet-Induced ob/ob Mouse Model of MASH},

author = {Di Pasqua LG and Palladini G and Croce AC and Milanesi G and Cavallo M and Adorini L and Ferrigno A and Vairetti M},

url = {https://www.mdpi.com/1422-0067/26/22/11023},

doi = {10.3390/ijms262211023},

year  = {2025},

date = {2025-12-22},

journal = {International journal of molecular sciences},

volume = {26},

issue = {2},

pages = {11023},

abstract = {This study evaluated the protective role of farnesoid-X-receptor (FXR) agonist INT-787 in the control of mitochondrial changes using a metabolic dysfunction-associated steatohepatitis (MASH) model. Lep-ob/ob mice were fed a control diet (CD) for 21 weeks (wks), or a high-fat diet (HFD) for 9 or 21 wks; in the 21 wk HFD groups, INT-787 (30 mg/kg/day) dosed via HFD admixture was added. The hepatic ATP, ROS, GSH and MIC19, which stabilizes the structure of inner mitochondrial membrane (IMM), were quantified. Transmission electron microscopy (TEM) analysis was also performed. INT-787 increased hepatic ATP, which was downregulated after HFD 9 and 21 wks. Hepatic ROS increased and GSH decreased after 21 wks and were recovered by INT-787. MIC19 mRNA level decreased after HFD 21 wks, and it was completely restored after INT-787 administration. TEM analysis showed that INT-787 reverted the mitochondrial alterations as documented by restored mitochondrial length, number of mitochondrial cristae junctions (CJs), and distance between endoplasmic reticulum (ER) and outer mitochondrial membrane (OMM) when compared with HFD groups. These results underline the involvement of the FXR pathway in the control of mitochondrial damage, thus revealing a previously undiscovered mechanism mediated by FXR activation: the upregulation of IMM protein MIC19, which is essential for maintaining cristae integrity and mitochondrial function.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_246,

title = {The E3 ligase RNF32 controls the IκB kinase complex and NF-κB signaling in intestinal stem cells},

author = {Lauriola A and Enrique Steinberg JH and Sarubo M and Maspero E and Rossi FA and Mouri Y and Pedretti M and Hajisadeghian M and Taibi V and Vettori A and Vitulo N and Assfalg M and D'Onofrio M and Rossi M and Yasue A and Astegno A and Polo S and Santi S and Kudo Y and Guardavaccaro D



},

url = {https://www.sciencedirect.com/science/article/pii/S1097276525008226?via%3Dihub},

doi = {10.1016/j.molcel.2025.10.005},

year  = {2025},

date = {2025-11-19},

journal = {Molecular cell},

abstract = {Nuclear factor κB (NF-κB) signaling is a central pathway regulating a plethora of cellular functions. Here, we find that RNF32, a RING E3 ubiquitin ligase whose expression is enriched in murine intestinal stem cells, regulates the activity of the IκB kinase (IKK) complex, the signal integration hub for NF-κB activation. The E3 ligase activity of RNF32 depends on calmodulin, the primary calcium sensor in eukaryotic cells. Increased levels of intracellular calcium ion (Ca2+) induce RNF32 binding to calmodulin, RNF32 activation, and autoubiquitylation. In turn, polyubiquitin chains conjugated to RNF32 recruit NEMO, the regulatory subunit of the IKK complex. Moreover, Ca2+ rise triggers RNF32 phase separation, which is required for the formation of NEMO condensates and IKK activation. Finally, we show that RNF32 is required for NF-κB activation triggered by bacterial lipopolysaccharides. Collectively, our findings uncover a mechanism controlling NF-κB signaling in the intestinal epithelium.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_244,

title = {In vitro and in vivo characterization of novel magnesium alloy implants enhanced by hydrothermal and sol-gel treatments for bone regeneration},

author = {Bellavia D and Paduano F and Brogini S and Ruggiero R and Marano RM and Cusanno A and Guglielmi P and Piccininni A and Pavarini M and D'Agostino A and Gambardella A and Peres C and Palumbo G and Chiesa R and Zappini G and Tatullo M and Giavaresi G},

url = {https://pubs.rsc.org/en/content/articlelanding/2025/tb/d5tb01282a},

doi = {10.1039/d5tb01282a},

year  = {2025},

date = {2025-11-19},

journal = {Journal of materials chemistry B},

abstract = {Magnesium alloys are emerging as promising materials for biodegradable orthopedic implants due to their mechanical strength and biocompatibility. However, their clinical use is hindered by rapid degradation and hydrogen gas evolution, which can compromise implant stability and bone healing. This study investigates the biocompatibility, genotoxicity, and osteointegration of magnesium implants (AZ31) produced via Superplastic Forming and enhanced through Hydrothermal and Sol-Gel surface treatments. Both techniques produced uniform Mg(OH)2-based coatings, but only alloy with hydrothermal treatment exhibited a markedly slower in vitro degradation. Cytotoxicity and Ames mutagenicity assays confirmed the biocompatibility and non-mutagenic nature of all implant types. In vivo evaluation in a rat femoral defect model revealed successful bone formation around all implant types, with comparable trabecular bone area. However, surface-treated implants showed a significantly lower bone-to-implant contact compared to the control AZ31 alloy, with solgel-treated alloys exhibiting an accelerated degradation rate and higher hydrogen release, which may influence tissue integration. These results highlight the role of surface modification in tuning degradation behavior and bone interface characteristics, with solgel-treated alloys resorbing faster. The combination of superplastic forming processing with strategic surface treatments offers a promising approach to achieving controlled biodegradation, although further optimization is needed to improve bone-implant integration. This work supports the further development of surface-engineered Mg implants for safe and functional orthopedic applications.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_243,

title = {Circular RNAs in Cardiovascular Physiopathology: From Molecular Mechanisms to Therapeutic Opportunities},

author = {Capirossi G and Brasini S and Tremoli E and Binatti A and Roncarati R},

url = {https://www.mdpi.com/1422-0067/26/19/9725},

doi = {10.3390/ijms26199725},

year  = {2025},

date = {2025-11-19},

journal = {International journal of molecular sciences},

volume = {26},

issue = {19},

pages = {9725},

abstract = {Circular RNAs are a class of stable non-coding RNAs generated through a back-splicing mechanism. They are now recognized as central players in cell function and are no longer considered byproducts of transcription. CircRNAs regulate gene expression at the transcriptional, post-transcriptional, and translational levels by interacting with various molecules. They act as sponges for miRNAs and proteins, molecular scaffolds, and can also be translated into peptides. Although advances in next-generation sequencing and PCR methods have improved their identification and quantification, technical and bioinformatic challenges remain. Increasing evidence shows their involvement in cardiovascular diseases such as heart failure, hypertrophy, fibrosis, and atherosclerosis, with protective or deleterious effects depending on the context. Given their presence in biological fluids and extracellular vesicles, they can be considered promising biomarkers, but their therapeutic applications are still under investigation. Future studies including a better understanding of their mechanisms of action, the development of standardized validation methods, and potential clinical applications (prevention, early diagnosis, personalized therapies) in diseases are still needed. This review provides an updated overview of the knowledge regarding circRNAs and their translational role in health and disease with a particular focus on cardiovascular diseases.},

note = {Review},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_242,

title = {Epidemiological and Clinical Data from the European lipodystrophy (ECLip) registry},

author = {Ceccarini G and Vatier C and Akinci B and Belalem I and Broekema M and Csajbok E and Rosaria D'Apice M and Gambineri A and Heldt K and Heni M and Kleinendorst L and Krause K and Lattanzi G and Miehle K and Palladino L and Prodam F and Santini F and Santos Silva E and Savage DB and Sbraccia P and Scherer T and Sorkina E and Stotl I and Vantyghem MC and Vigouroux C and Vorona E and Araujo-Vilar D and Wabitsch M and Nagel G and von Schnurbein J; ECLip Registry Consortium},

url = {https://academic.oup.com/ejendo/advance-article/doi/10.1093/ejendo/lvaf214/8305425?login=true},

doi = {10.1093/ejendo/lvaf214},

year  = {2025},

date = {2025-11-19},

journal = {European journal of endocrinology},

volume = {193},

issue = {5},

pages = {685-703},

abstract = {Objective: Lipodystrophy syndromes comprise a group of rare diseases characterized by loss of adipose tissue without nutritional or catabolic causes. As the rarity of these conditions necessitates collaboration, the European Consortium of Lipodystrophies (ECLip) established an international, longitudinal registry for patients with all forms of lipodystrophy (excluding HIV-associated cases). Methods: From December 2017 to November 2023, 19 centres from 13 countries recruited 631 patients into the ECLip registry. Cross-sectional data were analysed using descriptive statistics Results: Prospective data was available for 467 patients (82.7%, female; 86.5% adults; median age 44.0 years). Familial partial lipodystrophy (FPLD) was the most common subtype (57.4%), especially FPLD2 (37.9%). However, in men congenital generalized lipodystrophy was nearly as common as FPLD (33.3% vs. 35.8%). Symptoms at onset varied by subtype, with loss of adipose tissue being the most frequent. More than 70% of the patients suffered from metabolic complications, particularly dyslipidaemia (59.0%) and diabetes (48.4%) but prevalence and severity varied between subtypes (prevalence of diabetes for example 76.9% in patients with acquired partial lipodystrophy vs 8.7% in acquired localized lipodystrophy). Metreleptin, the only disease-specific treatment, was used by 11.6% of all patients. 34 deaths were documented, primarily due to cardiovascular events and cancer. Patients with generalized forms of lipodystrophy died earlier compared to patients with partial forms (median age at death 27.0 vs. 72.0 years). Conclusion: This study describes the largest cohort of patients with lipodystrophy reported to date. The dataset offers a comprehensive view of the epidemiology, clinical presentation, and associated comorbidities of lipodystrophy.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_241,

title = {Chromatin remodeling restrains oncogenic functions in prostate cancer},

author = {Rosti V and Lembo G and Petrini C and Gorini F and Quadri R and Cordiglieri C and Mutarelli M and Salviato E and Casari E and Di Patrizio Soldateschi E and Montanari E and Albo G and Ripa F and Fasciani A and Crosti M and De Lorenzis E and Maggioni M and Vaira V and Vivo M and Ferrari F and Lanzuolo C},

url = {https://www.nature.com/articles/s41467-025-64213-4},

doi = {10.1038/s41467-025-64213-4},

year  = {2025},

date = {2025-10-21},

journal = {Nature Communications},

volume = {16},

pages = {9174},

abstract = {Primary prostate cancer presents with multifocal lesions and unpredictable clinical behavior, posing significant challenges for effective prognosis. To address this, we investigate the epigenomic landscape of prostate tumor biopsies from 25 treatment-naïve male patients by analyzing chromatin compartmentalization patterns. Our analysis reveals two distinct molecular subtypes: one with a Low Degree of Decompartmentalization (LDD) and another with a High Degree of Decompartmentalization (HDD). Here we show that the HDD subgroup exhibits extensive chromatin reorganization associated with diminished oncogenic potential. This subtype shows repression of molecular pathways involved in extracellular matrix remodeling and cellular plasticity. From this distinction, we derive an 18-gene transcriptional signature capable of differentiating HDD from LDD cases. Importantly, we validate the prognostic relevance of this signature in multiple independent cohorts totaling over 900 patients. Our findings suggest that epigenetic-derived signature at the time of diagnostic biopsy can offer a powerful tool for risk stratification in prostate cancer.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_240,

title = {Spiroplasma impairs testes gene expression in Glossina fuscipes fuscipes},

author = {Piccinno R and Fiorenza G and Lescai F and Carpanzano S and Gstottenmayer F and Dera KM and Croce AC and de Beer CJ and Santorsola M and Gasperi G and Forneris F and Abd-Alla AMM and Aksoy S and Malacrida AR},

url = {https://www.biorxiv.org/content/10.1101/2025.09.23.678099v1},

doi = {10.1101/2025.09.23.678099},

year  = {2025},

date = {2025-10-21},

journal = {bioRxiv},

volume = {2025.09.23.678099},

abstract = {Glossina fuscipes fuscipes is a riverine tsetse fly species, the primary vector of human and animal trypanosomiasis in Sub-Saharan Africa. Controlling tsetse fly populations is crucial for mitigating the socio-economic impact of this disease, as effective treatments remain challenging. Indeed, the development of control strategies is hindered by the species' unique reproductive biology: adenotrophic viviparity, in which the female retains and nourishes the developing larva in her uterus throughout the pregnancy. The discovery of Spiroplasma in some G. f. fuscipes populations has drawn attention as a potential tool to enhance tsetse fly control strategies. Although Spiroplasma does not exhibit in G. f. fuscipes the male-killing phenotype observed in Drosophila melanogaster, evidence suggests that it may confer refractoriness to Trypanosoma infection. This has led to further investigations into its broader effects on G. f. fuscipes biology, particularly its potential impact on Glossina reproductive fitness. In this study, we considered Spiroplasma effect on the male reproduction. For this, we performed a differential gene expression analysis on testes and male accessory glands (MAGs) between Spiroplasma-infected and uninfected males. A significant downregulation of genes was observed in testes while a minor effect has been detected on MAGs. Downregulation of testes genes associated with functions related to sperm motility, energy metabolism, and mitochondrial function has been observed. Additionally, differentially expressed genes involved in antimicrobial activity and circadian rhythm regulation were observed. These findings provide valuable insights into the potential fitness costs of Spiroplasma infection for the fly and its implications for the bacterium use as biological control strategies targeting G. f. fuscipes.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_239,

title = {Spontaneous activity of astrocytes is a stochastic functional signal for memory consolidation},

author = {Losi G and Vignoli B and Granata R and Lia A and Zonta M and Sansevero G and Pischedda F and Chiavegato A and Santi S and Zentilin L and Berardi N and Ratto GM and Carmignoto G and Canossa M},

url = {https://www.pnas.org/doi/10.1073/pnas.2500511122?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub++0pubmed},

doi = {10.1073/pnas.2500511122},

year  = {2025},

date = {2025-10-21},

journal = {Proceedings of the National Academy of Sciences of the United States of America},

volume = {122},

issue = {42},

pages = {e2500511122},

abstract = {In the absence of explicit neuronal inputs, the glial cell astrocytes exhibit recurring intracellular Ca2+ fluctuations, primarily localized at thin processes, known as Ca2+ microdomains (MDs). Although spontaneous Ca2+ MDs are present throughout the brain, their putative role is unknown. Here, we question whether, owing to their recurring signaling mode, spontaneous Ca2+ MDs contribute to slowly evolving phenomena in the brain, such as memory consolidation. We demonstrate that, in the perirhinal cortex, a central region in recognition memory, these events promote Ca2+-dependent gliotransmission and modulate synaptic strengthening. Their recurring activity extends the release of the gliotransmitter brain-derived neurotrophic factor (BDNF) over time, ensuring the sustained Tropomyosin Receptor Kinase B (TrkB)-signaling required for the consolidation of long-term synaptic potentiation and lasting memories. We also show that Ca2+ MDs, which are stochastic events, preserve their random behavior during gliotransmission, introducing an element of unpredictability into the process of memory retention. Our study assigns to spontaneous, stochastic activity in astrocytes a unique functional role in shaping and stabilizing memory circuits.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_222,

title = {ANKRD2 Knockdown as a Therapeutic Strategy in Osteosarcoma: Effects on Proliferation and Drug Response in U2OS and HOS Cells},

author = {Cenni V and Bavelloni A and Capanni C and Mattioli E and Bortolozzo F and Kojic S and Orlandi G and Bertacchini J and Blalock WL},

url = {https://www.mdpi.com/1422-0067/26/4/1736},

doi = {10.3390/ijms26041736},

year  = {2025},

date = {2025-10-21},

urldate = {2025-08-11},

journal = {International journal of molecular sciences},

volume = {26},

issue = {4},

pages = {1736},

abstract = {Ankrd2, a mechanoresponsive protein primarily studied in muscle physiology, is emerging as a player in cancer progression. This study investigates the functional role of Ankrd2 in osteosarcoma cells, revealing its critical involvement in cell proliferation and response to chemotherapeutic drugs. We showed that Ankrd2 knockdown impairs the activation of PI3K/Akt and ERK1/2 pathways, reduces levels of cell cycle regulators including cyclin D1 and cyclin B, and counteracts the expression of nuclear lamin A and lamin B, disrupting nuclear morphology and DNA integrity. Strikingly, the loss of Ankrd2 enhances the sensitivity of osteosarcoma cells to doxorubicin and cisplatin, highlighting Ankrd2 potential as a therapeutic target to improve chemotherapeutic efficacy. Defining a novel mechanistic role for Ankrd2 in promoting tumor progression, we propose that Ankrd2 reduction could be exploited as an adjuvant strategy to enhance the efficacy of chemotherapy, offering new therapeutic opportunities for OS treatment.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_218,

title = {In vitro study of cold atmospheric plasma-induced proliferation inhibition and morphological changes in head and neck carcinoma cell lines},

author = {Maravic T and Petrucci G and Giacomo VD and Mazzitelli C and Acharya TR and Kaushik NK and Choi EH and Rapino M and D'Urso D and Josic U and Caponio VCA and Micaroni M and Edoardo M and Russo LL and Muzio LL and Breschi L and Perotti V},

url = {https://www.sciencedirect.com/science/article/pii/S0300571225004518?via%3Dihub},

doi = {10.1016/j.jdent.2025.106007},

year  = {2025},

date = {2025-10-21},

urldate = {2025-08-11},

journal = {Journal of dentistry},

volume = {161},

pages = {106007},

abstract = {"Objectives: The use of cold atmospheric plasma (CAP) has been growing in medical field. Since limited data exist on the influence of CAP exposure on head and neck cancer (HNC) cells, we aimed to investigate in vitro its impact on proliferation and morphology of HNC (HSC2, HSC3, and FaDu) cells, as well as healthy gingival fibroblasts (hGF).

Methods: A CAP gas air jet was applied directly on the HSC2, HSC3, FaDu and hGF cells for 30 and 60 s; doxorubicin has been used as positive control. Inhibition of cell proliferation at different time points (24, 48, and 72 h) was investigated through MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium]. Morphological alterations were observed using scanning electron microscope (SEM) and transmission electron microscope (TEM). Data were statistically analyzed (p < 0.05). Results: CAP exposure of 60 s showed the highest proliferation inhibitory effects in all investigated cancer cell lines (p < 0.001). While HSC2 had the highest proliferation inhibition at 24 h, HSC3, and FaDu exhibited a positive, time-dependent inhibitory effect (24 < 48 < 72 h) after CAP exposure. Interestingly, effects of CAP in the hGF were minimal. SEM observations revealed morphological changes in HNC cells treated with CAP at 30 and 60 s. Moreover, TEM showed stressed conditions in the survived HNC cells at 48 h after CAP exposure demonstrated by the presence of multilamellar and multi-vesicular bodies. Conclusions: CAP treatment induced proliferation inhibition, morphologic changes and stressed conditions in HNC cell lines (HSC2, HSC3, and FaDu), while demonstrating limited effects on hGF cells.Clinical significance: This work characterized early cellular responses of HSC2, HSC3, and FaDu to CAP exposure, including proliferation, and morphology, as foundational data before progressing to more clinically representative models."},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_215,

title = {Sammy Basso, his life and message, and the importance of progeria research},

author = {Lattanzi G},

url = {https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehaf355/8160766?login=true#google_vignette},

doi = {10.1093/eurheartj/ehaf355},

year  = {2025},

date = {2025-10-21},

urldate = {2025-08-11},

journal = {European heart journal},

volume = {46},

number = {2945-2946},

issue = {30},

abstract = {not available},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nokey,

title = {Trichothiodystrophy: Molecular insights and mechanisms of pathogenicity},

author = {Lanzafame M and Brevi F and Veniali G and Botta E},

url = {https://www.sciencedirect.com/science/article/pii/S1383574225000262?via%3Dihub},

doi = {10.1016/j.mrrev.2025.108555},

year  = {2025},

date = {2025-10-21},

urldate = {2025-08-11},

journal = {Mutation research. Reviews in mutation research},

volume = {796},

pages = {108555},

abstract = {Trichothiodystrophy (TTD) is a rare hereditary disease characterized by brittle, sulphur deficient hair associated with a wide and varied spectrum of clinical features which include skin alterations, neurodevelopmental defects, and immune dysfunction. The presence of hypersensitivity to UV light defines the two main forms of TTD: photosensitive (PS-TTD) and non-photosensitive (NPS-TTD). The disease arises from mutations in a variety of genes involved in different biological processes. Affected processes include DNA repair, transcription as well as translation. This review provides the latest vision of TTD: from up-to-date mutational spectra and genotype-phenotype relationships to our current understanding of the pathogenic mechanisms that underlie the complex etiology of this multi-faceted disease.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_238,

title = {DBR1 and the RNAopathy Landscape of Trichothiodystrophy},

author = {Veniali G and Lanzafame M},

url = {https://www.sciencedirect.com/science/article/abs/pii/S0022202X25023139?via%3Dihub},

doi = {10.1016/j.jid.2025.07.011},

year  = {2025},

date = {2025-10-10},

urldate = {2025-10-10},

journal = {Journal of investigative dermatology},

abstract = {not available - Commentary to "RNA Lariat-Debranching Enzyme (DBR1) Variations in Sabinas Brittle Hair Syndrome Form of Trichothiodystrophy: A Trichothiodystrophy-Causing Gene" Sikandar G. Khan, Wenelia Baghoomian,  Christiane Kuschal-Tauzon, Deborah Tamura, Maxwell P. Lee, John J. DiGiovanna, Rodrigo Cepeda-Valdes, Julio Salas-Alanis, Kenneth H. Kraemer (DOI: https://doi.org/10.1016/j.jid.2025.06.1591)},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_237,

title = {Proceedings of the annual meeting of the European Consortium of Lipodystrophies (ECLip) Paris, France, 20-21 May 2025},

author = {Vatier C and Araujo-Vilar D and Akinci B and Arnould T and Beaupère C and Bismuth E and Brown RJ and Ceccarini G and Collas P and Gambineri A and Gilio D and Halperin S and Janmaat S and Lamothe S and Lattanzi G and Maffei M and MacDougald OA and Mosbah H and Nobecourt E and Oral EA and Rochford J and Santini F and Schirmer EC and von Schnurbein J and Semple R and Tews D and Wabitsch M and Vantyghem MC and Vigouroux C},

url = {https://www.sciencedirect.com/science/article/pii/S0003426625007516?via%3Dihub},

doi = {10.1016/j.ando.2025.102432},

year  = {2025},

date = {2025-10-10},

journal = {Annales de endocrinologie},

volume = {86},

issue = {5},

pages = {102432},

abstract = {Lipodystrophy syndromes are rare diseases characterized by anatomical and functional defects of adipose tissue, frequently leading to severe insulin resistance-associated metabolic complications. Subtypes of lipodystrophy syndromes differ in: their clinical presentation, with generalized or partial loss of adipose tissue; in their origin, either genetic or acquired; and in their comorbidities, forming a heterogeneous group of disorders of different severity. The European Consortium of Lipodystrophies (ECLip) was founded in 2014 as a non-profit network of health professionals, scientists and patient associations. ECLip aims to promote international collaborations to increase pathophysiological and clinical knowledge, and improve the management of lipodystrophy syndromes. ECLip now comprises 59 groups from 30 countries from Europe and beyond. The consortium developed in parallel to the increased awareness of clinical diagnosis, the growing scientific interest for these diseases at the crossroads between adipose tissue biology, whole body metabolism, genetics and immunity, and to the emergence of new pharmacological approaches. The ECLip congress, held every 18 months, aims to discuss the recent achievements and projects in the field of lipodystrophies, to consolidate ECLip activities and to promote future collaborations, highlighting clinical and fundamental aspects as well as patients' perspectives. Oral communications presented during the meeting in Paris, France, in 2025 are summarized in these minutes.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_212,

title = {Fatty acid binding protein 1 (FABP1) depletion promotes an oxidative metabolic shift in Caco-2 colorectal cancer cells},

author = {Borus DL and Zadra G and Minsky D and Costa ML and Corsico B and Storch J and Scaglia N},

url = {https://www.sciencedirect.com/science/article/pii/S1388198125000691?via%3Dihub},

doi = {10.1016/j.bbalip.2025.159661},

year  = {2025},

date = {2025-10-06},

urldate = {2025-08-11},

journal = {Biochimica et biophysica acta. Molecular and cell biology of lipids},

volume = {1870},

issue = {7},

pages = {159661},

abstract = {Lipid metabolism reprogramming is a well-established hallmark of many cancer types, including colorectal cancer (CRC). Nevertheless, a clear understanding on how fatty acid (FA) metabolism is fine-tuned during CRC development and progression is still missing. Given that CRC is the second leading cause of cancer-related death, addressing these critical aspects may provide the rationale for new therapeutic approaches and early biomarker identification. Fatty acid binding protein 1 (FABP1) is a small protein that binds FA and other lipophilic compounds, acting as a lipid transporter in the intestine. Little is currently known about the function of FABP1 in CRC. Here we show that the knockdown of FABP1 in CRC cells impairs de novo FA and cholesterol synthesis, specifically, via altering the transcriptional regulation of lipid metabolism genes. FABP1 depletion suppresses the expression of FA and cholesterol synthesis-associated genes while promoting that of FA oxidation genes and mitochondrial oxidative pathways. The latter is associated with increased oxygen consumption rate and activation of the energy sensor 5' AMP-activated kinase (AMPK). Taken together, our results show that FABP1 orchestrates the balance between FA synthesis and oxidation, most likely to prevent the cytotoxic effects of circulating unbound free fatty acids. Thus, targeting FABP1 function may represent a potential therapeutic strategy in advanced CRC.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_236,

title = {Proceedings of the annual meeting of the European Consortium of Lipodystrophies (ECLip) Paris, France, 20-21 May 2025},

author = {Vatier C and Araujo-Vilar D and Akinci B and Arnould T and Beaupere C and Bismuth E and Brown RJ and Ceccarini G and Collas P and Gambineri A and Gilio D and Halperin S and Janmaat S and Lamothe S and Lattanzi G and Maffei M and MacDougald OA and Mosbah H and Nobecourt E and Oral EA and Rochford J and Santini F and Schirmer EC and von Schnurbein J and Semple R and Tews D and Wabitsch M and Vantyghem MC and Vigouroux C},

url = {https://www.sciencedirect.com/science/article/pii/S0003426625007516?via%3Dihub},

doi = {10.1016/j.ando.2025.102432},

year  = {2025},

date = {2025-09-29},

journal = {Annales de endocrinologie},

volume = {86},

issue = {5},

pages = {102432},

abstract = {Lipodystrophy syndromes are rare diseases characterized by anatomical and functional defects of adipose tissue, frequently leading to severe insulin resistance-associated metabolic complications. Subtypes of lipodystrophy syndromes differ in: their clinical presentation, with generalized or partial loss of adipose tissue; in their origin, either genetic or acquired; and in their comorbidities, forming a heterogeneous group of disorders of different severity. The European Consortium of Lipodystrophies (ECLip) was founded in 2014 as a non-profit network of health professionals, scientists and patient associations. ECLip aims to promote international collaborations to increase pathophysiological and clinical knowledge, and improve the management of lipodystrophy syndromes. ECLip now comprises 59 groups from 30 countries from Europe and beyond. The consortium developed in parallel to the increased awareness of clinical diagnosis, the growing scientific interest for these diseases at the crossroads between adipose tissue biology, whole body metabolism, genetics and immunity, and to the emergence of new pharmacological approaches. The ECLip congress, held every 18 months, aims to discuss the recent achievements and projects in the field of lipodystrophies, to consolidate ECLip activities and to promote future collaborations, highlighting clinical and fundamental aspects as well as patients' perspectives. Oral communications presented during the meeting in Paris, France, in 2025 are summarized in these minutes.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_233,

title = {Tracking micro- and nanoplastics in Aedes albopictus: From ingestion to metabolic disruption},

author = {Soldano S and Bonanomi M and Aramini T and Moyano A and Garbelli A and Croce AC and Weththimuni ML and Vaghi P and Puggioli A and Gomulski LM and Gaglio D and Scolari F},

doi = {10.1016/j.scitotenv.2025.180447},

year  = {2025},

date = {2025-09-29},

journal = {The Science of the total environment},

volume = {1002},

issue = {180447},

abstract = {Urban aquatic environments are increasingly contaminated with micro- and nanoplastics (MNLPs), posing risks to biodiversity and human health. These environments are ideal breeding sites for larvae of the Asian tiger mosquito Aedes albopictus, a key arbovirus vector. While plastic pollution is a global concern, physiological and metabolic consequences of MNPL-exposure in mosquitoes remain poorly understood. Combining epifluorescence and confocal imaging, mosquito life-history parameter assessment, and high-throughput metabolomic profiling, we investigated the effects of polystyrene MNPLs on Ae. albopictus. We demonstrated that ingested MNPLs cross the larval gut barrier, persist in various tissues, and are retained through development. Exposure did not significantly affect pre-imaginal survival or development time, but reduced larval body weight and caused profound metabolic alterations. Metabolomic analyses revealed downregulation of central carbon metabolism, particularly glycolysis and pentose phosphate pathway, alongside amino acid alterations linked to stress responses. Notably, MNPL-exposure also affected juvenile hormone biosynthesis, suggesting endocrine disruption. This trend was observed in both NP- and MP-exposed larvae, with a greater number of differentially regulated metabolites following MP-treatment. Interestingly, TCA cycle dysregulation was more pronounced in NP-exposed larvae, whereas perturbations in glutathione metabolism, amino sugar metabolism and nitrogen excretion were associated with MP-exposure. These findings highlight the metabolic and physiological consequences of MNPL-exposure, with potential implications for mosquito ecology, vector capacity, and environmental dissemination of plastic contaminants. Given the role of Ae. albopictus in disease transmission and its adaptation to urban habitats, further research is needed to explore the long-term ecological and epidemiological consequences of plastic pollution on mosquito populations.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_232,

title = {Telomeric DNA damage response mediates neurotoxicity of Aβ42 oligomers in Alzheimer's disease},

author = {Sepe S and Rey F and Mancheno-Ferris A and Bigi A and Fani G and Damiani D and Cabrini M and Marinelli E and Aguado J and Contu L and di Lillo A and Boggio S and Tavella S and Rosso I and Gustincich S and Chiti F and {d'Adda di Fagagna F},

doi = {10.1038/s44318-025-00521-1},

year  = {2025},

date = {2025-09-29},

urldate = {2025-09-29},

journal = {EMBO Journal},

volume = {44},

issue = {21},

pages = {6078-6111},

abstract = {Ageing is the major risk factor for Alzheimer's disease (AD), the most common neurodegenerative disorder. DNA damage is a hallmark of ageing, particularly when occurring at telomeres, genomic regions vulnerable to oxidative damage and often challenging for the cell to repair. Here, we show that brains of 3xTg-AD mice, an established AD model characterized by amyloid-β (Aβ)-induced pathology, exhibit increased activation of DNA damage response (DDR) pathways at telomeres. Exposure of mouse primary hippocampal neurons to 42-residue Aβ (Aβ42) oligomers, a significant pathogenetic contributor to AD, triggers telomeric DDR by increasing the levels of reactive oxygen species caused by calcium imbalance. Antisense oligonucleotides targeting non-coding RNAs generated at damaged telomeres in vivo (in 3xTg-AD mice) and in vitro reduce neurotoxicity in iPSC-derived human cortical neurons and mouse primary neurons while inhibiting Aβ42-induced telomeric DDR, and restore transcriptional pathways altered by Aβ and found dysregulated in AD patients. These results unveil an unexpected role of telomeric DNA damage responses in Alzheimer's disease pathogenesis, and suggest a novel target for the development of RNA-based therapies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_231,

title = {SOD-1/2 Involvement in the Antioxidant Molecular Events Occurring upon Complex Magnetic Fields Application in an In Vitro H2O2 Oxidative Stress-Induced Endothelial Cell Model},

author = {Ricci A and Zara S and di Giacomo V and Gallorini M and Rapino M and Di Pietro N and Cipollina A and Piattelli A and Cataldi A},

url = {https://www.mdpi.com/1422-0067/26/17/8600},

doi = {10.3390/ijms26178600},

year  = {2025},

date = {2025-09-29},

journal = {International journal of molecular sciences},

volume = {26},

issue = {17},

pages = {8600},

abstract = {"Endothelial function plays a key role in tissue repair. Reactive Oxygen Species (ROS) production impairs tissue renewal and homeostasis. Complex Magnetic Fields (CMFs) have been attracting attention as a non-invasive tool to promote tissue regeneration, especially through angiogenic stimulation. The present study aims to investigate CMF effect in an in vitro model of oxidative stress-stimulated Endothelial Cells (ECs). Cells were pre-treated with H2O2 to mimic an oxidative environment, followed by the application of three CMF programs repeated in two experimental sets: two consecutive cycles (two cycles) or two cycles spaced 24 h apart (T0+T24). Flow cytometry investigation shows that both CMF applications reduce ROS production, presumably promoting SODs proteins expression. Specifically, two cycles affect mitochondrial SOD-2 expression, which may promote cellular turnover by upregulating pro-apoptotic proteins, leading to mild cell death balanced with increased cell viability. T0+T24 application promotes cytosolic SOD-1 expression, which may influence the expression and release of antioxidant molecules, as evidenced by the increased protein levels of Akt/Nrf2 and the overall antioxidant activity measured post-treatment. In conclusion, ROS-induced EC dysfunction can be reverted by CMF application: 2 cycles could be applied when cellular renewal is required (such as in pathological wounds) while T0+T24 could be useful when an antioxidant and anti-inflammatory effect is needed (e.g., in edema or muscular lesions).},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y,

title = {Profibrotic Molecules Are Reduced in CRISPR-Edited Emery-Dreifuss Muscular Dystrophy Fibroblasts},

author = {Cattin E and Schena E and Mattioli E and Marcuzzo S and Bonanno S and Cavalcante P and Corradi F and Benati D and Farinazzo G and Cattaneo M and De Sanctis V and Bertorelli R and Maggi L and Giannotta M and Pini A and Vattemi G and Cassandrini D and Cavallo M and Manferdini C and Lisignoli G and Fontana B and Pace I and Bruno C and Roncarati R and Fiorillo C and Ferracin M and Schirmer EC and Recchia A and Lattanzi G

},

url = {https://www.mdpi.com/2073-4409/14/17/1321},

doi = {10.3390/cells14171321},

year  = {2025},

date = {2025-09-29},

urldate = {2025-09-29},

journal = {Cells},

volume = {14},

issue = {17},

pages = {1321},

abstract = {Emery-Dreifuss muscular dystrophy (EDMD) is caused by mutations in EMD, LMNA, SYNE1, SYNE2, and other related genes. The disease is characterized by joint contractures, muscle weakening and wasting, and heart conduction defects associated with dilated cardiomyopathy. Previous studies demonstrated the activation of fibrogenic molecules such as TGFbeta 2 and CTGF in preclinical models of EDMD2 and increased secretion of TGFbeta 2 in patient serum. A wide screening of patient cells suggested fibrosis, metabolism, and myogenic signaling as the most affected pathways in various EDMD forms. In this study, we show that alpha-smooth muscle actin-positive myofibroblasts are overrepresented in patient fibroblast cultures carrying EMD, LMNA, or SYNE2 mutations, and profibrotic miRNA-21 is upregulated. Upon CRISPR/Cas correction of the mutated EMD or LMNA sequence in EDMD1 or EDMD2 fibroblasts, respectively, we observe a reduced expression of fibrogenic molecules. However, in patient myoblasts, neither fibrogenic proteins nor miRNA-21 were upregulated; instead, miRNA-21-5p was downregulated along with muscle-specific miRNA-133b and miRNA-206, which have a crucial role in muscle cell homeostasis. These observations suggest that the conversion of laminopathic fibroblasts into a profibrotic phenotype is a determinant of EDMD-associated muscle fibrosis, while miRNA-206-dependent defects of laminopathic myoblasts, including altered regulation of VEGF levels, contribute to muscle cell deterioration. Notably, our study provides a proof-of-principle for the application of gene correction to EDMD1 and EDMD2 and presents EDMD1 isogenic cells that exhibit an almost complete rescue of a disease-specific miRNA signature. These cells can be used as experimental models for studying muscular laminopathies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_230,

title = {Developing Type II F508del-CFTR correctors with a protective effect against respiratory viruses},

author = {Barbieri F and Martina MG and Pesce E and Bianchi E and Cabella N and Crespan E and Rossi S and Gemma S and Campiani G and Milite C and Pepe G and Campiglia P and Sbardella G and Maga G and Cagno V and Pedemonte N and Radi M},

url = {https://www.sciencedirect.com/science/article/pii/S0223523425008633?via%3Dihub},

doi = {10.1016/j.ejmech.2025.118098},

year  = {2025},

date = {2025-09-29},

journal = {European journal of medicinal chemistry},

volume = {300},

pages = {118098},

abstract = {Cystic fibrosis (CF) is a multifaceted disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The resulting thick mucus accumulation increases the risk of microbial infections, leading to chronic lung inflammation, progressive tissue damage, and pulmonary exacerbations (PEs). Respiratory viruses may facilitate bacterial colonization, significantly contributing to PEs. Therefore, patients with CF could benefit from a timely antiviral treatment targeting respiratory viruses (e.g., rhinoviruses). Herein, we present novel multitarget agents that combine F508del-CFTR correction with broad-spectrum antiviral activity through inhibition of the host protein PI4KB, offering a promising therapeutic strategy to prevent pulmonary exacerbations in cystic fibrosis with no risk of developing antiviral drug resistance. Among the most active candidates, the bithiazole 3b showed broad-spectrum antiviral activity in the sub- or low-micromolar range against selected viruses from the Picornaviridae, Flaviviridae, and Coronaviridae families, and a notable F508del-CFTR correction-both alone and in combination with VX809-in FRT cells. Further confirmation of CFTR correction was obtained in the CFBE41o- cell line and in primary cultures of human airway epithelial cells homozygous for F508del, the gold standard for evaluating CFTR rescue strategies, particularly in combination with VX445. In addition to its biological activity, compound 3b exhibited a favorable preclinical pharmacokinetic profile in vitro. These findings collectively highlight compound 3b as a promising multitarget candidate for cystic fibrosis, providing a solid foundation for the development of a simplified CF therapy to mitigate PE.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_222,

title = {Polygenic prediction of body mass index and obesity through the life course and across ancestries},

author = {Smit RAJ and …… and Biino G and …… and Loos RJF},

url = {https://www.nature.com/articles/s41591-025-03827-z},

doi = {10.1038/s41591-025-03827-z},

year  = {2025},

date = {2025-09-29},

urldate = {2025-08-11},

journal = {Nature medicine},

volume = {31},

issue = {9},

pages = {3151-3168},

abstract = {Polygenic scores (PGSs) for body mass index (BMI) may guide early prevention and targeted treatment of obesity. Using genetic data from up to 5.1 million people (4.6% African ancestry, 14.4% American ancestry, 8.4% East Asian ancestry, 71.1% European ancestry and 1.5% South Asian ancestry) from the GIANT consortium and 23andMe, Inc., we developed ancestry-specific and multi-ancestry PGSs. The multi-ancestry score explained 17.6% of BMI variation among UK Biobank participants of European ancestry. For other populations, this ranged from 16% in East Asian-Americans to 2.2% in rural Ugandans. In the ALSPAC study, children with higher PGSs showed accelerated BMI gain from age 2.5 years to adolescence, with earlier adiposity rebound. Adding the PGS to predictors available at birth nearly doubled explained variance for BMI from age 5 onward (for example, from 11% to 21% at age 8). Up to age 5, adding the PGS to early-life BMI improved prediction of BMI at age 18 (for example, from 22% to 35% at age 5). Higher PGSs were associated with greater adult weight gain. In intensive lifestyle intervention trials, individuals with higher PGSs lost modestly more weight in the first year (0.55 kg per s.d.) but were more likely to regain it. Overall, these data show that PGSs have the potential to improve obesity prediction, particularly when implemented early in life.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_213,

title = {Defective collagen VI-NG2 axis impairs pericyte balance between proliferation and quiescence in COLVI-related myopathies},

author = {Fazio A and Sabatelli P and Faldini C and {Di Martino A} and Marvi MV and Neri I and Koufi FD and Merlini L and Manzoli L and Ratti S and Evangelisti C},

url = {https://www.sciencedirect.com/science/article/pii/S0925443925003606?via%3Dihub},

doi = {10.1016/j.bbadis.2025.168012},

year  = {2025},

date = {2025-09-29},

urldate = {2025-08-11},

journal = {Biochimica et biophysica acta. Molecular basis of disease},

volume = {1871},

issue = {8},

pages = {168012},

abstract = {Collagen VI-related myopathies (COLVI-RMs) are rare genetic disorders caused by impaired assembly and secretion of COLVI, a key extracellular matrix (ECM) protein. COLVI deficiency alters ECM architecture and biomechanics, leading to progressive muscle fiber damage and connective tissue abnormalities. While pericytes are emerging as key players in muscle regeneration due to their myogenic potential, their role in COLVI-RMs remains unclear. This study investigates pericyte involvement in COLVI-RMs, focusing on the interaction between COLVI and neural/glial antigen 2 (NG2), a proteoglycan expressed on pericyte membranes. Muscle biopsies from COLVI-RMs patients revealed abnormal pericyte distribution, reduced vessel coverage, and thickened capillary basement membranes. In vitro, healthy pericytes formed a dense COLVI network, while COLVI-RM-derived pericytes displayed a disrupted matrix and impaired cell-ECM interaction. Proximity ligation assays demonstrated a significant reduction in COLVI-NG2 binding in COLVI-RM pericytes, correlating with altered balance between proliferative and quiescent states. In turn, defects in signaling pathways related to proliferation (Akt/mTOR and Wnt/β-catenin pathways) and quiescence (N-cadherin, Notch3, FOXO3A) were identified, revealing a marked quiescent state. In vitro inhibition of the COLVI-NG2 binding in healthy pericytes reproduced these pathological features, underscoring the functional relevance of this molecular axis. Taken together, the data here reported revealed an unexpected role of NG2-COLVI binding on pericytes status. It follows that the impairment of functional binding between NG2 and COLVI could have important consequences on the pericytes myogenic potential in COLVI-RMs, and consequently on the muscle regeneration. Finally, targeting defective pericytes could provide potential therapeutic strategies for these debilitating diseases.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_229,

title = {In vitro study of cold atmospheric plasma-induced proliferation inhibition and morphological changes in head and neck carcinoma cell lines},

author = {Maravic T and Petrucci G and Giacomo VD and Mazzitelli C and Acharya TR and Kaushik NK and Choi EH and Rapino M and D'Urso D and Josic U and Caponio VCA and Micaroni M and Edoardo M and Russo LL and Muzio LL and Breschi L and Perotti V},

url = {https://www.sciencedirect.com/science/article/pii/S0300571225004518?via%3Dihub},

doi = {10.1016/j.jdent.2025.106007},

year  = {2025},

date = {2025-09-03},

journal = {Journal of dentistry},

volume = {161},

pages = {106007},

abstract = {Objectives: The use of cold atmospheric plasma (CAP) has been growing in medical field. Since limited data exist on the influence of CAP exposure on head and neck cancer (HNC) cells, we aimed to investigate in vitro its impact on proliferation and morphology of HNC (HSC2, HSC3, and FaDu) cells, as well as healthy gingival fibroblasts (hGF). Methods: A CAP gas air jet was applied directly on the HSC2, HSC3, FaDu and hGF cells for 30 and 60 s; doxorubicin has been used as positive control. Inhibition of cell proliferation at different time points (24, 48, and 72 h) was investigated through MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium]. Morphological alterations were observed using scanning electron microscope (SEM) and transmission electron microscope (TEM). Data were statistically analyzed (p < 0.05). Results: CAP exposure of 60 s showed the highest proliferation inhibitory effects in all investigated cancer cell lines (p < 0.001). While HSC2 had the highest proliferation inhibition at 24 h, HSC3, and FaDu exhibited a positive, time-dependent inhibitory effect (24 < 48 < 72 h) after CAP exposure. Interestingly, effects of CAP in the hGF were minimal. SEM observations revealed morphological changes in HNC cells treated with CAP at 30 and 60 s. Moreover, TEM showed stressed conditions in the survived HNC cells at 48 h after CAP exposure demonstrated by the presence of multilamellar and multi-vesicular bodies. Conclusions: CAP treatment induced proliferation inhibition, morphologic changes and stressed conditions in HNC cell lines (HSC2, HSC3, and FaDu), while demonstrating limited effects on hGF cells. Clinical significance: This work characterized early cellular responses of HSC2, HSC3, and FaDu to CAP exposure, including proliferation, and morphology, as foundational data before progressing to more clinically representative models.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_228,

title = {Human Helicase DDX5 is Hijacked by SARS-CoV‑2 Nsp13 Helicase to Enhance RNA Unwinding},

author = {Barra G and Ruggiero A and Napolitano V and Lodola C and Secchi M and Pallotta MM and Benincasa V and Leone F and Maga G and Berisio R},

url = {https://pmc.ncbi.nlm.nih.gov/articles/PMC12355267/},

doi = {10.1021/acsomega.5c04271},

year  = {2025},

date = {2025-09-03},

urldate = {2025-09-03},

journal = {ACS omega},

volume = {10},

issue = {31},

pages = {34941-34950},

abstract = {DEAD-box protein (DDX) 5 plays important roles in multiple aspects of cellular processes that require modulation of the RNA structure. Alongside the canonical role in RNA metabolism, numerous studies have demonstrated that DDX5 influences viral infections by directly interacting with viral proteins. However, the precise functional role of DDX5 during viral infection remains largely unclear. Here, we explore the previously undiscovered ability of DDX5 to interact and synergize with the Nsp13 helicase of SARS-CoV-2. We show that DDX5 exhibits a nanomolar binding affinity to Nsp13. Also, by dissecting DDX5 in its individual domains, we show that the Nsp13-DDX5 interaction is mediated by the RecA1 domain of DDX5. Importantly, we show that DDX5 and Nsp13 synergize in unwinding double-stranded RNA. Consistent with its ability to bind Nsp13, the RecA1 domain of DDX5 acts as a weak inhibitor of the synergic action of the two helicases in the RNA unwinding process. Modeling of the DDX5-Nsp13 complex provides a plausible explanation for the synergic action of the two helicases, in a mechanism that is likely instrumental in the early stage of infection, when the concentration of Nsp13 is still low.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_228,

title = {Weaponizing CRISPR/Cas9 for selective elimination of cells with an aberrant genome},

author = {Tavella S and di Lillo A and Conti A and Iannelli F and Mancheno-Ferris A and Matti V and Di Micco R and {d’Adda di Fagagna F}},

url = {https://www.sciencedirect.com/science/article/pii/S1568786425000369?via%3Dihub},

doi = {10.1016/j.dnarep.2025.103840},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

journal = {DNA Repair},

volume = {149},

pages = {103840},

abstract = {The CRISPR/Cas9 technology is a powerful and versatile tool to disrupt genes' functions by introducing sequence-specific DNA double-strand breaks (DSBs). Here, we repurpose this technology to eradicate aberrant cells by specifically targeting silent and non-functional genomic sequences present only in target cells to be eliminated. Indeed, an intrinsic challenge of most current therapies against cancer and viral infections is the non-specific toxicity that they can induce in normal tissues because of their impact on important cellular mechanisms shared, to different extents, between unhealthy and healthy cells. The CRISPR/Cas9 technology has potential to overcome this limitation; however, so far effectiveness of these approaches was made dependent on the targeting and inactivation of a functional gene product. Here, we generate proof-of-principle evidence by engineering HeLa and RKO cells with a promoterless Green Fluorescent Protein (GFP) construct. The integration of this construct simulates either a genomic alteration, as in cancer cells, or a silent proviral genome. Cas9-mediated DSBs in the GFP sequence activate the DNA damage response (DDR), reduce cell viability and increase mortality. This is associated with increased cell size, multinucleation, cGAS-positive micronuclei accumulation and the activation of an inflammatory response. Pharmacological inhibition of the DNA repair factor DNA-PK enhances cell death. These results demonstrate the therapeutic potential of the CRISPR/Cas9 system in eliminating cells with an aberrant genome, regardless of the expression or the function of the target DNA sequence.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_227,

title = {Transcription: friend or foe of genome stability},

author = {Compe E and Orioli D},

url = {https://febs.onlinelibrary.wiley.com/doi/10.1002/1873-3468.15091},

doi = {10.1002/1873-3468.15091},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

journal = {FEBS letters},

volume = {599},

issue = {2},

pages = {143-146},

abstract = {No abstract available},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_226,

title = {Sex Disparities in P53 Regulation and Functions: Novel Insights for Personalized Cancer Therapies},

author = {Cardano M and Buscemi G and Zannini L},

url = {https://www.mdpi.com/2073-4409/14/5/363},

doi = {10.3390/cells14050363},

year  = {2025},

date = {2025-08-11},

journal = {Cells},

volume = {14},

issue = {5},

pages = {363},

abstract = {Epidemiological studies have revealed significant sex differences in the incidence of tumors unrelated to reproductive functions, with females demonstrating a lesser risk and a better response to therapy than males. However, the reasons for these disparities are still unknown and cancer therapies are generally sex-unbiased. The tumor-suppressor protein p53 is a transcription factor that can activate the expression of multiple target genes mainly involved in the maintenance of genome stability and tumor prevention. It is encoded by TP53, which is the most-frequently mutated gene in human cancers and therefore constitutes an attractive target for therapy. Recently, evidence of sex differences has emerged in both p53 regulations and functions, possibly providing novel opportunities for personalized cancer medicine. Here, we will review and discuss current knowledge about sexual disparities in p53 pathways, their role in tumorigenesis and cancer progression, and their importance in the therapy choice process, finally highlighting the importance of considering sex contribution in both basic research and clinical practice.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_225,

title = {Effect of Spiroplasma infection on the mating behavior of Glossina fuscipes fuscipes},

author = {Fiorenza G and Piccinno R and Bruzzese DJ and Scolari F and Milanesi G and Casali C and Gomulski LM and Lescai F and Forneris F and Gasperi G and Dera KM and de Beer C and Abd-Alla AMM and Aksoy S and Malacrida AR},

url = {https://onlinelibrary.wiley.com/doi/10.1111/1744-7917.70042},

doi = {10.1111/1744-7917.70042},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

journal = {Insect science},

volume = {32},

issue = {5},

pages = {1726-1736},

abstract = {Tsetse flies are insects of significant public health and zoonotic importance as they are the main vectors of African trypanosomes. To date, an effective vaccine is unavailable and efforts to limit the spread of the disease primarily rely on controlling the tsetse populations. The discovery of Spiroplasma (class Mollicutes) in Glossina fuscipes fuscipes (Gff) (palpalis subgroup), offers promising insights into its potential use as a biological control agent to hinder trypanosomes infection in tsetse flies. Indeed, a negative correlation between Spiroplasma and trypanosome co-infection has been observed. Using a laboratory strain of Gff, we provide fundamental biological insights into the effects of Spiroplasma infection on the mating behavior of the fly. We found a sex-biased Spiroplasma infection, with males exhibiting a higher infection rate. Mass mating experiments revealed a higher mating propensity in Spiroplasma-infected flies. Additionally, the presence of Spiroplasma influenced premating isolation, leading to nonrandom mating patterns that favored the pairing of individuals with matching infection statuses. Moreover, we present evidence of Spiroplasma vertical paternal transmission. By analyzing female reproductive tissues at 2 and 24 h postmating, we confirmed that an infected male can transfer Spiroplasma to the female via the spermatophore, which can subsequently migrate to the spermathecae. This study provides foundational insights into the role of Spiroplasma in tsetse fly mating behavior and provides supporting evidence for vertical transmission from infected males.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_224,

title = {Circulating MicroRNAs in Patients with Psoriasis Treated with Anti-IL-23: A Cohort Study},

author = {Diotallevi F and Matacchione G and Campanati A and Marinelli Busilacchi E and Viola N and Pace I and Fontana B and Roncarati R and Bonafe' M and Ferracin M and Sabbatinelli J and Olivieri F},

url = {https://link.springer.com/article/10.1007/s13555-024-01331-9},

doi = {10.1007/s13555-024-01331-9},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

journal = {Dermatology and therapy},

volume = {15},

issue = {1},

pages = {125-140},

abstract = {Introduction: Psoriasis is characterized by aberrant keratinocyte activity and immune cell infiltration, driven by immune-mediated pathways. MicroRNAs (miRNAs) play crucial roles in regulating these processes, offering insights into disease mechanisms and therapeutic targets. Objectives: This study aimed to investigate changes in circulating miRNAs in psoriasis patients undergoing risankizumab therapy, an anti-IL-23 monoclonal antibody, to understand its impact on disease pathogenesis and treatment response. Methods: Plasma samples from 12 psoriasis patients were collected before (T0) and after 1 year (T1) of risankizumab treatment and analyzed using small RNA sequencing. Findings were validated in a separate cohort of 23 patients using quantitative real-time PCR (qRT-PCR). T-regulatory cell (Treg) numbers and pro-inflammatory cytokine levels were also assessed. Results: Significant clinical improvement was observed in all patients after 1 year of treatment, accompanied by increased Treg counts and reduced levels of pro-inflammatory cytokines. Twenty-four miRNAs exhibited differential expression post-treatment; 9 were downregulated and 15 upregulated. Notably, miR-200a-3p showed a significant correlation with baseline Psoriasis Area Severity Index (PASI), indicating its potential as a severity marker. Risankizumab therapy also decreased peripheral blood levels of IL-23, IL-1β, and IL-8. Conclusions: This study identifies specific circulating miRNAs, including miR-200a-3p, as potential biomarkers for monitoring treatment responses in psoriasis patients. The findings underscore the therapeutic efficacy of risankizumab in modulating miRNA profiles and immune pathways associated with psoriasis pathogenesis. Overall, these results provide new insights into the mechanisms of risankizumab action and highlight miRNAs as promising candidates for personalized medicine approaches in psoriasis management.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_223,

title = {Chemical Analysis of Plasma-Activated Culture Media by Ion Chromatography},

author = {Locatelli M and Perrucci M and Balaha M and Acharya TR and Kaushik NK and Choi EH and Rapino M and Perrotti V},

url = {https://www.mdpi.com/1424-8247/18/2/199},

doi = {10.3390/ph18020199},

year  = {2025},

date = {2025-08-11},

journal = {Pharmaceuticals (Basel)},

volume = {18},

issue = {2},

pages = {199},

abstract = {Background: Currently, the procedures and methods applied in biological and medical fields for the determination of reactive oxygen and nitrogen species (RONS), primarily rely on spectrophotometric techniques, which involve the use of colorimetric reagents. While these methods are widely accepted, they exhibit significant limitations from an analytical standpoint, particularly due to potential inaccuracies, artifacts, and pronounced susceptibility to matrix effects. The purpose of this Technical Note is to demonstrate the application of ion chromatography-a robust and well-established analytical technique-for the quantification of RONS produced in cell culture media through the exposure to cold atmospheric plasma (CAP), an innovative therapeutic approach for cancer treatment, known as CAP indirect treatment. In addition, the present protocol proposes to apply the pharmacokinetics principles to the RONS generated in plasma-treated liquids (PTLs) following CAP exposure. Methods: The strategy involves elucidating the kinetic profiles of certain characteristic species by evaluating their half-life in the specific media used for cell cultures and investigating their "pharmacokinetic" (PK) profile. In this approach the drug dose is represented by the plasma power and the infusion time corresponds to the exposure time of the culture medium to CAP. Volume-dependent results were shown, focusing on nitrites and nitrates activities, justifying cellular inhibition. Results: This methodology enables the correlation of the PTL biological effects on different cell lines with the PK profiles (dose/time) obtained via ion chromatography. Conclusions: In conclusion, being a simple and green method, it could be used as an alternative to toxic reactions and analytical techniques with higher detection limits, while achieving good resolution.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_223,

title = {FACILITY: feeding the family-the intergenerational approach to fight obesity, a cross-sectional study protocol},

author = {Vincenti and Calcaterra V and Santero S and Viroli G and Di Napoli I and Biino G and Daconto L and Cusumano M and Zuccotti G and Cena H},

url = {https://www.frontiersin.org/journals/pediatrics/articles/10.3389/fped.2025.1450324/full},

doi = {1450324},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

journal = {Frontiers in pediatrics},

volume = {13},

pages = {1450324},

abstract = {Introduction: Paediatric obesity has been described by the World Health Organization as one of the most serious health challenges of the 21st century. Over the past four decades, the number of children and adolescents with obesity has increased between 10 and 12-fold worldwide. Methods: Childhood obesity is a complex and multifactorial outcome which can be attributed to factors such as socioeconomic status, ethnicity, lifestyle and eating habits. Beside personal-children-related factors, maternal (education, food knowledge, income) and environmental ones (food environment's features and accessibility) have been proven but their influences are still worth discussion. The cross-sectional study of the "FACILITY: feeding the family-the intergenerational approach to fight obesity" project aims at estimating children prevalence of overweight and obesity and assessing the impacts of lifestyle and of socio-economic-cultural and environmental factors on overweight and obesity. Results: Due to the current importance of developing multidisciplinary mother-child centred prevention programs, FACILITY cross-sectional study will investigate maternal and child socio-cultural, economic, environmental, health and lifestyle-related risk factors for the development of obesity. Discussion: The knowledge gained will provide the basis to develop a "primordial prevention program" to early tackle childhood obesity. Clinical trial registration: ClinicalTrials.gov, identifier (NCT06179381).},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_221,

title = {Anti-myogenic and profibrotic effect of serum from patients affected by muscular laminopathies},

author = {Schena E and Pini A and Cavalcante P and Siciliano G and Ricci G},

url = {https://www.actamyologica.it/article/view/1126},

doi = {10.36185/2532-1900-1126},

year  = {2025},

date = {2025-08-11},

journal = {Acta myologica: myopathies and cardiomyopathies: official journal of the Mediterranean Society of Myology },

abstract = {Emery-Dreifuss Muscular Dystrophy type 2 (EDMD2) and LMNA-related congenital muscular dystrophy (L-CMD) are caused by mutations in LMNA gene. Both pathologies are characterized by joint contractures, muscle weakness and wasting and cardiac involvement. In the last few years, circulating factors have been proposed to play a critical role in the pathogenesis of these diseases. Based on this consideration, we studied the effect of laminopathic serum on the myogenic differentiation in healthy human myoblasts in culture. We observed impaired myogenesis and increased fibrosis in myoblast cultures conditioned with laminopathic serum and a dramatic increase in the level of profibrotic and proinflammatory cytokines in the cell culture supernatants. These results strongly support the pathogenic role of circulating factors in muscular laminopathies and pave the way to a possible therapeutic strategy.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_220,

title = {DNA damage response defects induced by the formation of TDP-43 and mutant FUS cytoplasmic inclusions and their pharmacological rescue},

author = {Modafferi S and Farina S and Esposito F and Brandi O and Di Salvio M and Della Valle I and D'Uva S and Scarian E and Cicio G and Riccardi A and Pisati F and Garbelli A and Santini T and Pansarasa O and Morlando M and D'Ambrosi N and Cozzolino M and Cestra G and {d'Adda di Fagagna F} and Gioia U and Francia S},

url = {https://www.nature.com/articles/s41418-025-01530-7},

doi = {10.1038/s41418-025-01530-7},

year  = {2025},

date = {2025-08-11},

journal = {Cell death and differentiation},

abstract = {Formation of cytoplasmic inclusions (CIs) of TDP-43 and FUS, along with DNA damage accumulation, is a hallmark of affected motor neurons in Amyotrophic Lateral Sclerosis (ALS). However, the impact of CIs on DNA damage response (DDR) and repair in this pathology remains unprobed. Here, we show that CIs of TDP-43 and FUSP525L, co-localizing with stress granules, lead to a dysfunctional DDR activation associated with physical DNA breakage. Inhibition of the activity of the DDR kinase ATM, but not of ATR, abolishes DDR signaling, indicating that DNA double-strand breaks (DSBs) are the primary source of DDR activation. In addition, cells with TDP-43 and FUSP525L CIs exhibit reduced DNA damage-induced RNA synthesis at DSBs. We previously showed that the two endoribonucleases DROSHA and DICER, also known to interact with TDP-43 and FUS during small RNA processing, contribute to DDR signaling at DSBs. Treatment with enoxacin, which stimulates DDR and repair by boosting the enzymatic activity of DICER, restores a proficient DDR and reduces DNA damage accumulation in cultured cells with CIs and in vivo in a murine model of ALS. In Drosophila melanogaster, Dicer-2 overexpression rescues TDP-43-mediated retinal degeneration. In summary, our results indicate that the harmful effects caused by TDP-43 and FUS CIs include genotoxic stress and that the pharmacological stimulation of the DNA damage signaling and repair counteracts it.},

keywords = {},

pubstate = {forthcoming},

tppubtype = {article}

}

@article{%a1.%Y_219,

title = {Myopathic Ehlers-Danlos Syndrome (mEDS) Related to COL12A1: Two Novel Families and Literature Review},

author = {Merlini L and Sabatelli P and Cenni V and Zanobio M and Di Martino A and Traina F and Faldini C and Nigro V and Torella A},

url = {https://www.mdpi.com/1422-0067/26/11/5387},

doi = {10.3390/ijms26115387},

year  = {2025},

date = {2025-08-11},

journal = {International journal of molecular sciences},

volume = {26},

issue = {11},

pages = {5387},

abstract = {Myopathic Ehlers-Danlos syndrome (RmEDS) is an emerging hybrid phenotype that combines connective and muscle tissue abnormalities. It has been associated with variants of the COL12A1 gene, which are known as Ullrich congenital muscular dystrophy-2 (UCMD2; 616470) and Bethlem myopathy-2 (BTHLM2; 616471). Here, we report two splicing mutations of COL12A1 identified in three patients from two unrelated families who present a combination of joint hypermobility and axial, distal, and proximal weakness. The muscular strength of their neck and limb muscles was assessed at 4/5 (MRC); however, when measured with a myometer, the expected percentage by age and sex ranged from 35% to 40% for elbow flexion, 37% to 75% for knee extension, and was 50% for neck flexion. In addition to confirming the characteristic atrophy of the rectus femoris, we presented evidence of involvement of the neck and lumbar muscles through MRI and CT imaging. In vitro studies revealed filamentous disorganization and an altered pattern of collagen XII alpha 1 chain migration due to the skipping of exons 55 and 56 of collagen XII. Additionally, we review the myopathic involvement of COL12-RM in 30 patients across 18 families with dominant mutations and 15 patients from 13 families with recessive mutations.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y,

title = {Exploring structure-activity relationships of pyrrolyl diketo acid derivatives as non-nucleoside inhibitors of terminal deoxynucleotidyl transferase enzyme},

author = {Madia VN and Garibaldi N and Ialongo D and Patacchini E and Tudino V and Ruggieri G and Zarbo L and Cara E and Coluccia A and Artico M and Scipione L and Messore A and Saccoliti F and Mentegari E and Maga G and Di Santo R and Crespan E and Costi R},

url = {https://www.tandfonline.com/doi/full/10.1080/14756366.2025.2496782?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org},

doi = {10.1080/14756366.2025.2496782},

year  = {2025},

date = {2025-08-11},

journal = {Journal of enzyme inhibition and medicinal chemistry},

volume = {40},

number = {1},

abstract = {Terminal deoxynucleotidyl transferase (TdT) is overexpressed in some cancer types, where it drives the mutagenic repair of double strand breaks through non canonical non-homologous end joining pathway. The TdT enzyme belongs to the X family of polymerases, together with the DNA polymerase λ (pol λ) and β (pol β). However, TdT exclusively displays template-independent nucleotide polymerisation. Pursuing our studies in developing TdT inhibitors, herein we deepened the structure-activity relationships of new structural analogues of our previously identified hit compounds. The diketo hexenoic acid derivatives here analysed showed high selectivity towards TdT and inhibition potencies spanning from the low micromolar range to the nanomolar. Docking studies highlighted the chemical features involved in the TdT binding, well contributing to the rationalisation of the structural requirements needed for the enzymatic inhibition.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_216,

title = {Mapping of RORγt+ dendritic cells in human tissues establishes their preferential niche in adult lymph nodes},

author = {Lonardi S and Bianchetto-Aguilera FM and Monti M and {Di Matteo A} and Missale F and Picinoli S and Bugatti M and Benedetti M and Ferrari G and Cassatella MA and Moratto D and Zini S and Agostini V and Savoldi V and Lorenzi L and Chiarini M and Facchetti F and Wu S and Antonova AU and Liu YA and Cella M and Ghigna C and Colonna M and Vermi W},

url = {https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2025.1527499/full},

doi = {1527499},

year  = {2025},

date = {2025-08-11},

urldate = {2025-08-11},

journal = {Frontiers in immunology},

volume = {16},

pages = {1527499},

abstract = {Background: The retinoic-acid-receptor-related orphan receptor gamma t (RORγt) isoform is required for the development of lymphoid organs, T-helper 17 cells (Th17), and innate lymphoid cells (ILC3s). Recent data in mouse and human have revealed non-T, non-ILC3 cell populations with antigen presenting features that express RORγt. This study maps the presence of RORγt cells with dendritic cell (DC) features in human adult and fetal lymphoid tissues. Methods: By combining multicolor flow cytometry, RNAseq of peripheral blood cells, analysis of lymph node scRNAseq datasets, and microscopic analysis on human tissue sections and single-cell suspensions, this study maps the presence of RORγt cells with DC features in human tissues. Results: RORγt-DCs are found in human lymphoid organs, particularly in lymph nodes. Lymph node RORγt-DCs are located in the interfollicular area surrounding high endothelial venules and in the marginal sinuses. In terms of phenotype, RORγt-DCs are distinct from other nodal dendritic cells. They express PRDM16 and PIGR as well as transcripts supporting the antigen presentation machinery, while lacking stromal markers. A significant fraction of RORγt-DCs is proliferating, suggesting local self-renewal. Moreover, most of them lack autoimmune regulator (AIRE) expression. Comparison with mouse RORγt Thetis cells (TC) and Janus cells (JC) shows more similarity with group II TC than group I and III TC or JC, all of which are tolerogenic and express AIRE. Conclusion: Overall, this study identifies human lymph nodes as a relevant niche for RORγt-DCs and establishes tools for their microscopic mapping in human disease states},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_214,

title = {Trichothiodystrophy-causative pathogenic variants impair a cooperative action of TFIIH and DDX1 in R-loop processing},

author = {Ferri D and Branca G and Lanzafame M and Gandolfi E and Riva V and Maga G and Nardo T and Landi C and Bini L and Arseni L and Peverali FA and Compe E and Orioli D},

url = {https://academic.oup.com/nar/article/53/14/gkaf745/8221718?login=true},

doi = {10.1093/nar/gkaf745},

year  = {2025},

date = {2025-08-11},

journal = {Nucleic Acids Research},

volume = {53},

issue = {14},

pages = {gkaf745},

abstract = {The transcription factor IIH (TFIIH) is a key player in transcription and DNA repair by nucleotide excision repair. It is made of 10 subunits organized in core-TFIIH and CAK sub-complexes bridged by XPD. Pathogenic variants in the ERCC2/XPD gene give rise to xeroderma pigmentosum (XP) or trichothiodystrophy (TTD), two distinct clinical entities with opposite skin cancer proneness. Here, we show that TTD variants cause a partial dissociation of the CAK from the chromatin and from the core-TFIIH. Mass spectrometry analysis reveals that the chromatin-bound CAK, as a component of the entire TFIIH, participates in a protein assembly containing the RNA-binding proteins DDX1, SFPQ, NONO as well as RNA polymerase II (Pol II). Gene silencing experiments demonstrate that the protein assembly is required to process the DNA:RNA hybrids formed during Pol II extension and to protect the cell from transcriptional stress. TTD-specific variants in ERCC2/XPD result in TFIIH instability, altered interaction of the CAK with DDX1-SFPQ-NONO, and R-loop accumulation. Therefore, the limited amount of TFIIH that distinguishes TTD from XP gives rise to transcriptional stress and extensive gene expression deregulations, thus accounting for the wide spectrum of TTD clinical features.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{%a1.%Y_209,

title = {Combining prelamin A accumulation and oxidative stress: A strategy to target glioblastoma},

author = {Marvi MV and Evangelisti C and Cerchier CB and Fazio A and Neri I and Koufi FD and Blalock WL and Cenni V and Zoli M and Asioli S and Morandi L and Franceschi E and Manzoli L and Capanni C and Ratti S},

url = {https://www.sciencedirect.com/science/article/pii/S0171933525000160?via%3Dihub},

doi = {10.1016/j.ejcb.2025.151491},

year  = {2025},

date = {2025-06-10},

urldate = {2025-06-10},

journal = {European journal of cell biology},

volume = {104},

issue = {2},

pages = {151491},

abstract = {Glioblastoma is the most aggressive and prevalent tumor of the Central Nervous System (CNS) with limited treatment options and poor patient outcomes. Standard therapies, including surgery, radiation, and chemotherapy, provide only modest survival benefits, highlighting the need for innovative therapeutic approaches. This study investigates a novel strategy targeting prelamin A processing in glioblastoma cells. By inhibiting the farnesyltransferase enzyme using SCH66336 (Lonafarnib), we promote the accumulation of lamin A precursor (prelamin A) in glioblastoma cells, thereby increasing their susceptibility to oxidative stress induced by Menadione administration, while sparing normal human astrocytes. Notably, the combined SCH66336-Menadione treatment reduced cell proliferation, modified the expression of stemness markers, and decreased viability in patient-derived glioblastoma stem cells, which represent the population responsible for tumor aggressiveness and recurrence. These findings indicate that inhibiting prelamin A processing could be a potential strategy to reduce glioblastoma aggressiveness and enhance therapeutic outcomes, particularly for treatment-resistant glioblastoma stem cell populations. This approach shows potential for integrating prelamin A processing disruption as a complementary strategy in glioblastoma therapy.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}