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. 2022 May 31;9:868632. doi: 10.3389/fcvm.2022.868632

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Copyright © 2022 Wang, Park, Geng, Chen, Yang, Jiang, Yi, Tan, Zhou, Bian, Ma and Zhu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ROS plays a role in regulating the interaction between MG53 and RIPK1 in the injured myocardium. (A) The cardiac protective action of rhMG53 was determined by CK lease assay. The beneficial effects of rhMG53 treatment were blunted by treatments of low dose (50 mg/kg, NAC L) and high dose (250 mg/kg, NAC H) of NAC (n = 6 per group for control, NAC low dose and NAC high dose). The animals in all experimental groups were treated with rhMG53. (B) NAC (50 mg/kg) was injected (IP) into mice before ischemia and reperfusion. Interaction between MG53 and RIPK1 in injured myocardium was determined by co-immunoprecipitation with MG53 antibody and western blot analysis of RIPK1, RIPK3, MLKL, and MG53, the key component of necroptosis complex. (n = 3 per group for control and NAC treatment). IP, immunoprecipitation samples; WTE, whole tissue extraction samples.