Critical roles of m6A methylation in cardiovascular diseases

Xinmin Zhang; He Cai; He Xu; Su Dong; Haichun Ma

doi:10.3389/fcvm.2023.1187514

Critical roles of m⁶A methylation in cardiovascular diseases

Front Cardiovasc Med. 2023 May 19:10:1187514. doi: 10.3389/fcvm.2023.1187514. eCollection 2023.

Authors

Xinmin Zhang^{1

2}, He Cai³, He Xu⁴, Su Dong¹, Haichun Ma¹

Affiliations

¹ Department of Anesthesiology, The First Hospital of Jilin University, Changchun, China.
² The Public Laboratory Platform of the First Hospital of Jilin University, Changchun, China.
³ The Cardiovascular Center, The First Hospital of Jilin University, Changchun, China.
⁴ Department of Integrative Medicine, Lequn Branch, The First Hospital of Jilin University, Changchun, China.

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.

Keywords: cardiac hypertrophy; cardiovascular diseases; epigenetic; heart failure; ischemic heart disease; m6A methylation.

Publication types

Review

Grants and funding

This work was supported by grants from the National Natural Science Foundation of China (81970228), JiLin Province Science and Technology Development Plan (20210101353JC).