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. 2022 Apr 25;9:821317. doi: 10.3389/fcvm.2022.821317

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Copyright © 2022 Guo, Fan, Liu, Ma, An, Yang, Wang, Yang and Tang.

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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NEU1 knockdown attenuated mitochondrial deficiencies and ROS accumulation post-MI. (A) Enzymatic activity of mitochondrial electron transport chain enzymes (I, II, III, and IV) in isolated mitochondria from four groups of mice (n = 6). (B) Relative mitochondrial DNA content (mtDNA: nDNA) of heart (n = 6). (C) ATP content of cardiomyocytes in fresh heart (n = 6). (D) Mitochondrial ROS is assessed by MnSOD activity of fresh heart (n = 6). (E) ROS production in myocardial detected by DHE in fresh heart tissues. (F–H) Western blot image and quantitative results of the SIRT1/PGC1α pathway, the MFN2, and DRP1 of each group in vivo (n = 6). *p < 0.05 vs. Sham+shRNA group, #p < 0.05 vs. MI+shRNA group.