Critical roles of m
Xinmin Zhang1,2, He Cai3, He Xu4
1Department of Anesthesiology, The First Hospital of Jilin University, Changchun, China.
Insights
N6-methyladenosine (m6A) methylation is crucial in cardiovascular diseases (CVDs). This review explores m6A
Area of Science:
- Molecular Biology
- Epigenetics
- Cardiology
Background:
- Cardiovascular diseases (CVDs) are a leading global cause of mortality, with complex and not fully understood pathogenesis.
- N6-methyladenosine (m6A) methylation, the most prevalent mRNA epigenetic modification, is increasingly recognized for its role in cardiac physiology and pathology.
- m6A modifications are regulated by writers, erasers, and readers, influencing various cellular processes.
Purpose of the Study:
- To review the molecular functions of m6A enzymes in the context of cardiovascular diseases.
- To elucidate m6A-associated mechanisms and functions, particularly in heart failure and ischemic heart disease.
- To discuss the potential clinical applications and translation of m6A modifications in CVDs.
Main Methods:
- Literature review focusing on m6A methylation in cardiovascular research.
- Analysis of molecular mechanisms linking m6A to cardiac function and dysfunction.
- Synthesis of current understanding of m6A's role in heart failure and ischemia.
Main Results:
- m6A methylation influences critical cardiac processes including calcium homeostasis, endothelial function, cell death, autophagy, ER stress, and inflammation.
- Specific m6A enzymes (writers, erasers, readers) play significant roles in the development and progression of CVDs.
- m6A dysregulation is implicated in the pathogenesis of heart failure and ischemic heart disease.
Conclusions:
- m6A epigenetic modifications are integral to cardiovascular health and disease.
- Targeting m6A pathways presents a promising avenue for novel therapeutic strategies in CVDs.
- Further research into m6A modification holds potential for clinical transformation in managing cardiovascular conditions.
Abstract:
Cardiovascular diseases (CVDs) have been established as a major cause of mortality globally. However, the exact pathogenesis remains obscure. N6-methyladenosine (m6A) methylation is the most common epigenetic modification on mRNAs regulated by methyltransferase complexes (writers), demethylase transferases (erasers) and binding proteins (readers). It is now understood that m6A is a major player in physiological and pathological cardiac processes. m6A methylation are potentially involved in many mechanisms, for instance, regulation of calcium homeostasis, endothelial function, different forms of cell death, autophagy, endoplasmic reticulum stress, macrophage response and inflammation. In this review, we will summarize the molecular functions of m6A enzymes. We mainly focus on m6A-associated mechanisms and functions in CVDs, especially in heart failure and ischemia heart disease. We will also discuss the potential application and clinical transformation of m6A modification.
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