{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gao X"],"funding":["Heilongjiang Graduate Excellence Funding Program","National Natural Science Foundation of China","the Natural Science Foundation of Heilongjiang"],"pagination":["e05270"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12631900"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(43)"],"pubmed_abstract":["The clinical utility of the anticancer agent doxorubicin (DOX) is limited by its dose-dependent cardiotoxicity. ALYREF, a nuclear protein that preserves genomic stability through interactions with intranuclear components or as an m⁵C-binding regulator of mRNA maturation and export, has not been previously implicated in DOX-induced cardiotoxicity (DIC). Here, the role and underlying mechanisms of ALYREF in the pathogenesis of DIC are investigated. The findings demonstrate that ALYREF expression is markedly reduced in a murine model of DIC. Myocardial-specific overexpression of ALYREF attenuates DOX-induced DNA damage and cardiomyocyte apoptosis, whereas cardiac-specific knockout of ALYREF (ALYREF CKO) exacerbates DOX-induced cardiac dysfunction. Mechanistically, it is identified that nuclea"],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["Preservation of ALYREF Phase Separation Mitigates Doxorubicin-Induced Cardiomyocyte DNA Damage and Cardiotoxicity."],"pmcid":["PMC12631900"],"funding_grant_id":["82400418","PL2024H083","LJYXL2024-072","ZL2024H017;PL2024H083","82373958","ZL2024H017","82470266","82500435"],"pubmed_authors":["Li H","Yu L","Pan Z","Gong R","Xiao Z","Ren Z","Yang B","Han Z","Ma W","Liu X","Cai B","Cai A","Liu Y","Lian G","Tian Y","Zagidullin N","Gao X","Wang X","Shen Y"],"additional_accession":[]},"is_claimable":false,"name":"Preservation of ALYREF Phase Separation Mitigates Doxorubicin-Induced Cardiomyocyte DNA Damage and Cardiotoxicity.","description":"The clinical utility of the anticancer agent doxorubicin (DOX) is limited by its dose-dependent cardiotoxicity. ALYREF, a nuclear protein that preserves genomic stability through interactions with intranuclear components or as an m⁵C-binding regulator of mRNA maturation and export, has not been previously implicated in DOX-induced cardiotoxicity (DIC). Here, the role and underlying mechanisms of ALYREF in the pathogenesis of DIC are investigated. The findings demonstrate that ALYREF expression is markedly reduced in a murine model of DIC. Myocardial-specific overexpression of ALYREF attenuates DOX-induced DNA damage and cardiomyocyte apoptosis, whereas cardiac-specific knockout of ALYREF (ALYREF CKO) exacerbates DOX-induced cardiac dysfunction. Mechanistically, it is identified that nuclea","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-05T17:07:35.571Z","creation":"2026-05-19T03:12:02.861Z"},"accession":"S-EPMC12631900","cross_references":{"pubmed":["40899520"],"doi":["10.1002/advs.202505270"]}}