Abstract
Cardiovascular diseases (CVDs) represent the largest contributor to mortality worldwide. Identification of novel therapeutic targets and biomarkers for CVDs is urgently needed. Circular RNAs (circRNAs) are endogenous, abundant, and stable non-coding RNAs formed by back-splicing events. Their role as regulators of gene expression has been increasingly reported. Notably, circRNAs mediate essential physiological and pathological processes in the cardiovascular system. Our first aim, therefore, is to summarize recent advances in the role of circRNAs in cardiac development as well as in pathogenesis of various CVDs. Because circRNAs are stable in circulation and their dynamic changes may reflect different disease stages, they are considered ideal biomarkers. Therefore, our second aim is to review studies that have identified circulating circRNAs as biomarkers for CVDs. Finally, we discuss the shortage of functional studies and the limitations of available clinical studies and provide future perspectives.
Highlights
Cardiovascular diseases (CVDs) represent the largest contributor to mortality worldwide, leading to almost half of the 36 million annual deaths due to non-communicable diseases in the world.[1]
CircRNAs are generally divided into three types: circRNA derived from exons, circRNA derived from lariat introns, and circRNA derived from exons with retained introns (EIciRNA).[12,13,14]
Heart-related circRNA (HRCR) could act as a sponge for miR-223 and protect against cardiac hypertrophy and heart failure (HF) by inhibiting miR-223 activity.[20] and RNA co-immunoprecipitated with endogenous Ago[2] was analyzed in neonatal rat cardiomyocytes (CMs).[16] circRNAs were found to be highly enriched in the cytoplasm compared to linear transcripts.[16]
Summary
Yihua Bei,[1] Tingting Yang,[1] Lijun Wang,[1] Paul Holvoet,[2] Saumya Das,[3] Joost P.G. CircRNAs in Myocardial Infarction Myocardial infarction (MI) is a common manifestation of coronary artery disease (CAD) and represents a major cause of death among all CVDs.[46] ciRS-7, termed as Cdr1as, contains more than 70 conserved miR-7 target sites, reducing miR-7 activity and increasing target genes of miR-7.18 Expression of human Cdr1as in zebrafish had the similar effect of reducing miR-7, which impaired midbrain development.[47] ciRS-7 and its sponged miR-7 have been reported in cancer development.[48,49] Interestingly, Cdr1as and miR-7a were both increased in an MI mouse model and hypoxiatreated CMs,[50] which may be due to the fact that Cdr1as could regulate miR-7 stability at posttranscriptional level.[27] In mouse cardiac myocyte (MCM) cell line, Cdr1as overexpression could increase cell apoptosis, and this effect was inhibited by overexpression of miR-7a.50. Silencing cZNF609 increased endothelial cell viability, proliferation, migration, and tube formation at baseline and partially reduced oxidative or hypoxic stress-induced cell apoptosis in HUVECs.[61] miR-615-5p was predicated to be sponged by cZNF609, and miR-615-5p/cZNF609
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