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<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> Graphical Abstract <p>METTL3-mediated RNA m<sup>6</sup>A modification regulates heart diseases</p> <p>This review analyses the mechanisms and applications of METTL3 in heart diseases (myocardial infarction, myocardial ischemia/reperfusion injury, cardiac hypertrophy, and cardiac fibrosis), as well as targeting METTL3 for myocardial regeneration after heart failure.</p> <p>Methyltransferase-like 3 (METTL3). N<sup>6</sup>-methyladenosine (m<sup>6</sup>A). Oxidized low-density lipoprotein (ox-LDL). Angiotensin (Ang II). Vascular endothelial growth factor (VEGF). Reactive oxygen species (ROS). Ischemia/reperfusion (I/R). Extracellular matrix (ECM).</p> <p></p>

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METTL3-mediated m⁶A methylation in cardiac diseases: pathogenic roles and therapeutic potential

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月20日

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  • Ruida Liu,
  • Xiaojuan Su,
  • Lei Yang,
  • Dongqiong Xiao

摘要

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.

Graphical Abstract

METTL3-mediated RNA m6A modification regulates heart diseases

This review analyses the mechanisms and applications of METTL3 in heart diseases (myocardial infarction, myocardial ischemia/reperfusion injury, cardiac hypertrophy, and cardiac fibrosis), as well as targeting METTL3 for myocardial regeneration after heart failure.

Methyltransferase-like 3 (METTL3). N6-methyladenosine (m6A). Oxidized low-density lipoprotein (ox-LDL). Angiotensin (Ang II). Vascular endothelial growth factor (VEGF). Reactive oxygen species (ROS). Ischemia/reperfusion (I/R). Extracellular matrix (ECM).