N6-Methyladenosine RNA Methylation in Cardiovascular Diseases

Chi Liu; Lei Gu; Wenjuan Deng; Qianchao Meng; Nan Li; Guifeng Dai; Suli Yu; Hong Fang

doi:10.3389/fcvm.2022.887838

N6-Methyladenosine RNA Methylation in Cardiovascular Diseases

Front Cardiovasc Med. 2022 Apr 29:9:887838. doi: 10.3389/fcvm.2022.887838. eCollection 2022.

Authors

Chi Liu^{1

2}, Lei Gu³, Wenjuan Deng², Qianchao Meng⁴, Nan Li², Guifeng Dai², Suli Yu⁵, Hong Fang¹

Affiliations

¹ Department of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
² Department of Geriatrics Center, National Clinical Research Center for Aging and Medicine, Jing'an District Central Hospital of Shanghai, Fudan University, Shanghai, China.
³ Department of Internal Medicine, Shanghai Shende Hospital, Shanghai, China.
⁴ Innovation Research Institute of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
⁵ Department of Hand and Upper Extremity Surgery and Limb Function Reconstruction Center, Jing'an District Central Hospital, Shanghai, China.

Abstract

N6-methyladenosine (m6A) modification is the most universal and abundant post-transcriptional modification of eukaryotic RNA and occurs mainly at the consensus motif RR (m6A) CH (R = A or G, H = A, C, or U) in long internal exons, near stop codons, or in the 3' untranslated region (UTR). "Writers," "erasers," and "readers" are responsible for the occurrence, removal, and recognition of m6A modification, respectively. Substantial evidence has shown that m6A RNA modification can exert important functions in physiological and pathological processes. Cardiovascular diseases (CVDs) are a wide array of disorders affecting heart or vessels, including atherosclerosis (AS), hypertension (HT), ischemia/reperfusion (I/R) injury, myocardial infarction (MI), stroke, cardiac hypertrophy, heart failure (HF), and so on. Despite the advances in lipid-lowering drugs, antihypertensives, antiplatelet agents, and anticoagulation therapy, CVDs are still the leading cause of death worldwide. Recent studies have suggested that m6A modification of RNA may contribute to the pathogenesis of CVDs, providing a novel research insight for CVDs. Herein, we provide an up-of-date summarization of the molecular mechanism of m6A and the roles of m6A in different types of CVDs. At last, we propose that m6A might be a potiential biomarker or therapeutic target for CVDs.

Keywords: N6-methyladenosine; biomarkers; cardiovascular diseases; molecular mechanism; therapeutic target.

Publication types

Review