{"title":"METTL3-mediated m⁶A methylation in cardiac diseases: pathogenic roles and therapeutic potential.","authors":"Ruida Liu, Xiaojuan Su, Lei Yang, Dongqiong Xiao","doi":"10.1007/s10565-025-10039-1","DOIUrl":null,"url":null,"abstract":"<p><p>Cardiac dysfunction is a leading cause of death each year, putting heavy burdens on the global healthcare system. To improve our understanding of cardiac disease, novel perspectives for exploring their pathogenesis mechanisms are needed, which contributes to finding novel diagnoses and therapy targets for cardiac disease. To be noteworthy, researchers have paid great attention to understanding the pathogenesis of cardiac diseases from the perspective of methyltransferase-like 3 (METTL3, the catalytic core)-mediated RNA N<sup>6</sup>-methyladenosine modification and targeting METTL3 for therapy. Therefore, we aim to evaluate the significance of METTL3 in cardiac diseases. In the present review, we summarize and analyze all studies reporting the involvement of METTL3 in cardiac diseases (acute myocardial infarction, myocardial ischemia/reperfusion injury, cardiac hypertrophy, and cardiac fibrosis) to interpret their interrelationship. This review suggests that METTL3 is a risk gene for cardiac diseases, which shows great promise as a disease diagnosis and prognosis biomarker and is poised to serve as an important target in drug development. Collectively, this review presents a comprehensive, cutting-edge overview of METTL3 in cardiac diseases, which could be a valuable reference for researchers to understand disease pathogenesis and develop novel drugs.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"87"},"PeriodicalIF":5.3000,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12092566/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Biology and Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s10565-025-10039-1","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Cardiac dysfunction is a leading cause of death each year, putting heavy burdens on the global healthcare system. To improve our understanding of cardiac disease, novel perspectives for exploring their pathogenesis mechanisms are needed, which contributes to finding novel diagnoses and therapy targets for cardiac disease. To be noteworthy, researchers have paid great attention to understanding the pathogenesis of cardiac diseases from the perspective of methyltransferase-like 3 (METTL3, the catalytic core)-mediated RNA N6-methyladenosine modification and targeting METTL3 for therapy. Therefore, we aim to evaluate the significance of METTL3 in cardiac diseases. In the present review, we summarize and analyze all studies reporting the involvement of METTL3 in cardiac diseases (acute myocardial infarction, myocardial ischemia/reperfusion injury, cardiac hypertrophy, and cardiac fibrosis) to interpret their interrelationship. This review suggests that METTL3 is a risk gene for cardiac diseases, which shows great promise as a disease diagnosis and prognosis biomarker and is poised to serve as an important target in drug development. Collectively, this review presents a comprehensive, cutting-edge overview of METTL3 in cardiac diseases, which could be a valuable reference for researchers to understand disease pathogenesis and develop novel drugs.
期刊介绍:
Cell Biology and Toxicology (CBT) is an international journal focused on clinical and translational research with an emphasis on molecular and cell biology, genetic and epigenetic heterogeneity, drug discovery and development, and molecular pharmacology and toxicology. CBT has a disease-specific scope prioritizing publications on gene and protein-based regulation, intracellular signaling pathway dysfunction, cell type-specific function, and systems in biomedicine in drug discovery and development. CBT publishes original articles with outstanding, innovative and significant findings, important reviews on recent research advances and issues of high current interest, opinion articles of leading edge science, and rapid communication or reports, on molecular mechanisms and therapies in diseases.