Related Experiment Video
Updated: Jul 9, 2026
Methodology for Accurate Detection of Mitochondrial DNA Methylation
Published on: May 20, 2018
METTL3-mediated m⁶A methylation in cardiac diseases: pathogenic roles and therapeutic potential
Ruida Liu1,2, Xiaojuan Su1,3, Lei Yang4,5
1Department of Pediatrics/Key Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Insights
Methyltransferase-like 3 (METTL3) plays a key role in cardiac diseases. This review highlights METTL3 as a promising biomarker for diagnosis and prognosis and a potential therapeutic target for heart conditions.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Epigenetics
Background:
- Cardiac dysfunction is a major global health concern, necessitating novel insights into disease pathogenesis.
- RNA N6-methyladenosine (m6A) modification, particularly mediated by methyltransferase-like 3 (METTL3), is emerging as a critical factor in various biological processes.
- Understanding the role of METTL3 in the heart is crucial for developing new diagnostic and therapeutic strategies for cardiac diseases.
Purpose of the Study:
- To comprehensively review and analyze the current literature on the involvement of METTL3 in cardiac diseases.
- To elucidate the interrelationship between METTL3 and various cardiac pathologies.
- To evaluate the potential of METTL3 as a biomarker and therapeutic target in cardiovascular medicine.
Main Methods:
- Systematic review and analysis of published studies.
- Examination of research investigating METTL3's role in acute myocardial infarction, ischemia/reperfusion injury, cardiac hypertrophy, and cardiac fibrosis.
- Synthesis of findings to establish the significance of METTL3 in cardiac disease pathogenesis.
Main Results:
- METTL3 is implicated in the pathogenesis of multiple cardiac conditions, including acute myocardial infarction, ischemia/reperfusion injury, cardiac hypertrophy, and fibrosis.
- Evidence suggests METTL3 acts as a risk gene in the development of cardiac diseases.
- METTL3 demonstrates potential as a diagnostic and prognostic biomarker for cardiac dysfunction.
Conclusions:
- METTL3 is a significant player in the development and progression of cardiac diseases.
- METTL3 holds promise as a valuable biomarker for diagnosing and predicting the prognosis of cardiac conditions.
- Targeting METTL3 presents a promising avenue for novel drug development in cardiovascular therapeutics.
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.
Related Concept Videos
01:46Epigenetic Regulation
02:23Master Transcription Regulators
01:17Phase II Reactions: Methylation Reactions
The mechanism of methylation unfolds in two stages. The first stage sees a methyltransferase enzyme facilitating the transfer of a methyl group from S-adenosylmethionine (SAM) to the substrate, forming S-adenosylhomocysteine (SAH). The second stage involves further metabolism of SAH into homocysteine, which can be recycled...