Molecular mechanism of CAIF inhibiting myocardial infarction by sponging miR-488 and regulating AVEN expression

In recent years, the global incidence and mortality of myocardial infarction (MI) has increased and become one of the important diseases threatening public health. Long non-coding (lnc)RNAs are a type of ncRNA that serve critical roles in the progression of various types of disease. The present study aimed to investigate the effect and mechanism of lncRNA cardiac autophagy inhibitory factor (CAIF) on cardiac ischemia/reperfusion (I/R) injury. CAIF was downregulated in the myocardium of I/R rats and cardiomyocytes treated with hydrogen peroxide (H(2)O(2)). Further experiments demonstrated that CAIF overexpression inhibited I/R-induced cardiac infarction and apoptosis in vivo. CAIF decreased H(2)O(2)-induced apoptosis and oxidative stress of cardiomyocytes. Mechanistically, CAIF sponged microRNA (miR)-488-5p; this interaction was confirmed by rescue experiments. Moreover, miR-488-5p targeted apoptosis and caspase activation inhibitor (AVEN) and inhibited its expression. In summary, the present data identified a novel CAIF/miR-488-5p/AVEN signaling axis as a key regulator of myocyte apoptosis, which may be a potential therapeutic target for the treatment of MI.