Original ArticleCirc-HIPK2 Accelerates Cell Apoptosis and Autophagy in Myocardial Oxidative Injury by Sponging miR-485-5p and Targeting ATG101Zhou, Junling MM; Li, Longwei MM; Hu, Hao MM; Wu, Jiawei MM; Chen, Hongwu MM; Feng, Kefu MM; Ma, Likun MDAuthor Information Department of Cardiovascular, the First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China. Reprints: Likun Ma, MD, Department of Cardiovascular, the First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, NO. 1 Swan Lake Rd, Hefei 230001, Anhui, China (e-mail: email@example.com). Supported by the National Natural Science Foundation of China (NO. 81870192). The authors report no conflicts of interest. Journal of Cardiovascular Pharmacology: October 2020 - Volume 76 - Issue 4 - p 427-436 doi: 10.1097/FJC.0000000000000879 Buy Metrics Abstract Myocardial injury has been deemed as a major cause of heart diseases including myocarditis and coronary heart disease, which have brought multiple mortalities globally. Long non-coding RNAs (lncRNAs) are widely recognized in diverse diseases. However, the role of circular RNA HIPK2 (circ-HIPK2) remains unclear in myocardial injury induced by H2O2. We attempted to investigate the probable role of circ-HIPK2 in myocardial injury induced by H2O2. This study discovered that the treatment of H2O2 inhibited cell proliferation but boosted cell apoptosis and autophagy. ATG101 was upregulated in primary mouse neonatal cardiomyocytes under H2O2 treatment. ATG101 knockdown promoted proliferation and limited apoptosis by attenuating autophagy in H2O2-injured mouse neonatal cardiomyocytes. Furthermore, miR-485-5p was validated to combine with ATG101 and circ-HIPK2, and circ-HIPK2 positively regulated ATG101 expression by sponging miR-485-5p. At last, silenced circ-HIPK2 mediated the promotion of cell proliferation, and repression of cell apoptosis was restored by ATG101 amplification. In a word, circ-HIPK2 facilitates autophagy to accelerate cell apoptosis and cell death in H2O2-caused myocardial oxidative injury through the miR-485-5p/ATG101 pathway, indicating a novel therapeutic target point for patients with myocardial injury. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.