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.

The term "autophagy" was first proposed by the Nobel laureate Christian de Duve in 1963 to describe a cellular process which is highly conserved in eukaryotes to degrade or recycle cytoplasmic components through lysosomes. 1 According to the way in which materials are delivered to the lysosome, autophagy has been classified into three main types -macroautophagy, microautophagy, and

Circular RNAs (circRNAs), a novel class of non-coding RNA, are produced by back-splicing and were initially considered to be by-products of splicing. In recent years, computational technology and experimental evidence have revealed the tremendous amounts and potential physiological or pathological functions of this novel non-coding RNA species. At present, the roles of circRNAs in neurological diseases, immune diseases, and cancers have come to light. In addition, increasing studies have identified the expression profiles of circRNA in cardiovascular diseases (CVDs) and revealed the involvement of circRNAs in the pathogenesis of CVDs which are the leading cause of mortality and morbidity worldwide, and result in substantial health and financial burden. Despite current improvements in diagnostic and therapeutic approaches, survival and prognosis of CVDs patients remain relatively poor. Due to the involvements of circRNAs in CVDs and their outstanding characteristics of high stability, conservation, and tissue-or developmental-specificity, circRNA-based biomarkers or gene therapy may be effective approaches to reduce CVDs burden. In the review, we systematically summarized the formation mechanisms, functional models, and research approaches of circRNAs, and several circRNAs involved in CVDs. Finally, we proposed that developing circRNAs as biomarkers or circRNA-based therapeutic strategies based on biological or physical materials may be promising to diagnose or treat CVDs in the future.