<HashMap><database>biostudies-literature</database><scores/><additional><submitter>He Y</submitter><funding>National Natural Science Foundation of China</funding><pagination>e70829</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12413310</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>29(17)</volume><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</pubmed_abstract><journal>Journal of cellular and molecular medicine</journal><pubmed_title>METTL3 Silencing Suppresses Cardiac Fibrosis Post Myocardial Infarction via m6A Modification of SMOC2.</pubmed_title><pmcid>PMC12413310</pmcid><funding_grant_id>81400225</funding_grant_id><funding_grant_id>82000382</funding_grant_id><funding_grant_id>82300560</funding_grant_id><pubmed_authors>Pan X</pubmed_authors><pubmed_authors>Tao Z</pubmed_authors><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>Ling S</pubmed_authors><pubmed_authors>Sheng Z</pubmed_authors><pubmed_authors>He Y</pubmed_authors><pubmed_authors>Chen Z</pubmed_authors><pubmed_authors>Hao C</pubmed_authors><pubmed_authors>Song J</pubmed_authors><pubmed_authors>Zuo P</pubmed_authors><pubmed_authors>Ma G</pubmed_authors></additional><is_claimable>false</is_claimable><name>METTL3 Silencing Suppresses Cardiac Fibrosis Post Myocardial Infarction via m6A Modification of SMOC2.</name><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</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-06-03T02:15:24.438Z</modification><creation>2026-05-28T03:05:57.095Z</creation></dates><accession>S-EPMC12413310</accession><cross_references><pubmed>40913254</pubmed><doi>10.1111/jcmm.70829</doi></cross_references></HashMap>