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. 2022 Mar 16;2022:6023710. doi: 10.1155/2022/6023710

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Copyright © 2022 Xin Yi et al.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Oxidative stress under the regulation of histone methylation is increasingly being recognized as a target for cardioprotection in MIRI. The upregulation of NOX2/4 and iNOS modulated by KDM3A and ASH, respectively, contributes to oxidative stress in the development of MIRI. The transcription of SOD1/2 and HO-1 is regulated by SUV39h1 and SEDT7, respectively, which accelerates the degradation and removal of ROS in MIRI (ASH: absent small and homeotic; BRG1: Brahma-Related Gene-1; HO-1: heme oxygenase-1; Keap1: Kelch-like ECH-associated protein 1; KDM3A: lysine demethylase 3A; MIRI: myocardial ischemia-reperfusion injury; MRTF-A: myocardin-related transcription factor A; Nrf-2: nuclear factor erythroid 2-related factor 2; NOX2/4: NADPH oxidase 2/4; ROS: reactive oxygen species; SETD7: SET domain containing lysine methyltransferase 7; SIRT1: Sirtuin-1; SOD1/2: superoxide dismutase 1/2; SUV39h1: suppressor of variegation 3-9 homolog 1; TIP60: Tat-interacting protein 60).