LncRNA 0003250 accelerates heart autophagy and binds to miR‐17‐5p as a competitive endogenous RNA in chicken induced by selenium deficiency

Long noncoding RNAs (LncRNAs) have been demonstrated to be associated with a variety of myocardial diseases, but how LncRNAs regulate autophagy in selenium (Se)‐deficient myocardial injury is infrequently reported. Here, we screened out a novel long noncoding RNA, microRNA, and ATG7 through transcriptomic results. We employed a Se‐deficient chicken model in vivo, and primary cultured cardiomyocytes treated by correlation in vitro. The results showed that Se deficiency upregulated the expression of ATG7, and miR‐17‐5p inhibited cardiomyocyte autophagy by targeting ATG7. Furthermore, we found that LncRNA 0003250 regulated miR‐17‐5p, and thus affected the expression of ATG7 and autophagic cell death. Our present study proposed a novel model for the regulation of cardiomyocytes autophagy, which includes LncRNA 0003250, miR‐17‐5p and ATG7 in the chicken heart. Our conclusions may provide a feasible diagnostic tool for Se‐deficient cardiomyocyte injury. 1. The mechanism of selenium‐induced cardiomyocyte injury was first described at the molecular level. 2. The first discovery of the regulation of ceRNA mechanisms in selenium‐deficient cardiomyocytes 3. We proposed a novel regulating model of cardiomyocyte autophagy, which include LncRNA ATG7, miR‐17‐5p and ATG7 in the chicken heart.