Abstract
CircRNA, mainly derived from exons, lacks coding ability for the absence of 5’ Cap and 3’ poly (A) tail. Increasing evidence indicated that circRNA is closely associated with cardiovascular diseases via sponging miRNAs. However, few studies focused on the role of polypeptides from circRNA in heart. Here, we identified a circRNA (circ-Cdyl2) from CDYL2 (Chromodomain Y-like 2) increasing remarkably in vitro (hypoxia and low-glucose treated cardiomyocytes) or in vivo (failing heart post MI (myocardial infarction)) and coding a polypeptide termed Cdyl2-60aa for the presence of IRES (Internal Ribosomal Entry Sites). Cdyl2-60aa could stabilize the APAF1 (apoptotic protease activating factor-1) via blocking its interaction with HSP70 (heated shock protein 70) and in turn accelerated cell apoptosis. Results in vivo showed that the reduction of circ-Cdyl2 could significantly slow the deterioration of cardiac function post MI. In conclusion, our work discovered that circ-Cdyl2 promotes cell apoptosis via Cdyl2-60aa/APAF1 axis.
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