{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["He Y"],"funding":["National Natural Science Foundation of China"],"pagination":["e70829"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12413310"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(17)"],"pubmed_abstract":["Cardiac fibrosis, especially in the infarct border zone, leads to decreased cardiac compliance, impaired systolic and diastolic function, resulting in heart failure. M6A methylation plays a role in fibrosis development. However, its underlying mechanism remains poorly understood. This study explores the role and molecular mechanisms of m6A methylation in regulating cardiac fibrosis after myocardial infarction (MI). A mouse myocardial fibrosis model post-MI was established by ligating the left coronary artery. Corresponding gene knockdown was achieved in vitro or in vivo using short hairpin RNA or fibroblast-specific AAV9 virus. Echocardiography assessed cardiac function in mice, while Masson staining determined the degree of collagen deposition post-MI. The meRIP-Seq kit detected mRNA meth"],"journal":["Journal of cellular and molecular medicine"],"pubmed_title":["METTL3 Silencing Suppresses Cardiac Fibrosis Post Myocardial Infarction via m6A Modification of SMOC2."],"pmcid":["PMC12413310"],"funding_grant_id":["81400225","82000382","82300560"],"pubmed_authors":["Pan X","Tao Z","Liu Z","Ling S","Sheng Z","He Y","Chen Z","Hao C","Song J","Zuo P","Ma G"],"additional_accession":[]},"is_claimable":false,"name":"METTL3 Silencing Suppresses Cardiac Fibrosis Post Myocardial Infarction via m6A Modification of SMOC2.","description":"Cardiac fibrosis, especially in the infarct border zone, leads to decreased cardiac compliance, impaired systolic and diastolic function, resulting in heart failure. M6A methylation plays a role in fibrosis development. However, its underlying mechanism remains poorly understood. This study explores the role and molecular mechanisms of m6A methylation in regulating cardiac fibrosis after myocardial infarction (MI). A mouse myocardial fibrosis model post-MI was established by ligating the left coronary artery. Corresponding gene knockdown was achieved in vitro or in vivo using short hairpin RNA or fibroblast-specific AAV9 virus. Echocardiography assessed cardiac function in mice, while Masson staining determined the degree of collagen deposition post-MI. The meRIP-Seq kit detected mRNA meth","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-03T02:15:24.438Z","creation":"2026-05-28T03:05:57.095Z"},"accession":"S-EPMC12413310","cross_references":{"pubmed":["40913254"],"doi":["10.1111/jcmm.70829"]}}