Department of Cardiovascular Medicine, Huizhou Third People's Hospital, Guangzhou Medical University, Huizhou, Guangdong, China.
Shock. 2024 May 1;61(5):675-684. doi: 10.1097/SHK.0000000000002244. Epub 2023 Nov 16.
Myocardial 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.
心肌缺血再灌注损伤（MIRI）是心血管疾病的重要危险因素。一些环状 RNA 已被鉴定为 MIRI 的调节剂。然而，circ-mitochondrial amidoxime reducing component 2（circ-MARC2）在 MIRI 中的作用尚不清楚。我们的结果表明，circ-MARC2 在缺氧/复氧（H/R）处理的 AC16 细胞中过表达。circ-MARC2 沉默逆转了 H/R 处理对 AC16 细胞增殖的抑制作用，并促进了乳酸脱氢酶活性、肌酸激酶活性和细胞凋亡。此外，circ-MARC2 作为 miR-335-5p 的海绵，通过诱饵 miR-335-5p 减轻 H/R 诱导的 AC16 细胞损伤。此外，瞬时受体电位阳离子通道亚家族 M 成员 7（TRPM7）被鉴定为 miR-335-5p 的靶基因。miR-335-5p 的过表达缓解了 H/R 诱导的 AC16 细胞损伤，而 TRPM7 的升高则消除了这种作用。circ-MARC2 敲低通过 miR-335-5p/TRPM7 轴缓解 H/R 诱导的 AC16 细胞损伤。
