• Huazhao Deng, Meihong Cui, Ling Liu, and Fei Yang.
• Department of Cardiovascular Medicine, Huizhou Third People's Hospital, Guangzhou Medical University, Huizhou, Guangdong, China.
• Shock. 2024 May 1; 61 (5): 675684675-684.

AbstractMyocardial ischemia-reperfusion injury (MIRI) is a vital risk factor for cardiovascular diseases. Some circular RNAs have been identified as modulators of MIRI. However, the effects of circ-mitochondrial amidoxime reducing component 2 (circ-MARC2) in MIRI are unclear. Our results showed that circ-MARC2 was overexpressed in hypoxia/reoxygenation (H/R)-treated AC16 cells. Circ-MARC2 silencing reversed the inhibitory effect of H/R treatment on cell proliferation and promoting effects on lactate dehydrogenase activity, creatine kinase activity, and cell apoptosis in AC16 cells. Moreover, circ-MARC2 served as the sponge for miR-335-5p and ameliorated H/R-induced AC16 cell damage by decoying miR-335-5p. In addition, transient receptor potential cation channel subfamily M member 7 (TRPM7) was identified as the target gene of miR-335-5p. Overexpression of miR-335-5p relieved H/R-induced AC16 cell damage, whereas TRPM7 elevation abolished the effect. Circ-MARC2 knockdown was able to relieve H/R-induced AC16 cell injury through miR-335-5p/TRPM7 axis.Copyright © 2023 by the Shock Society.

39 keywords...

hide…