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. 2022 Jan 7;12:138. doi: 10.1038/s41598-021-03947-9

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Elimination of CPNS1 improves oxidative phosphorylation and decreases susceptibility to MPTP opening following ISC–REP. Compared to time control, ISC–REP decreased the rate of oxidative phosphorylation in both WT and KO (knockout) using glutamate + malate as complex I substrates (a). However, the extent of the decrease in oxidative phosphorylation was less in KO mitochondria following ISC–REP compared to WT (a), suggesting that elimination of CPNS1 attenuated complex I damage during ISC–REP. The ISC–REP led to decreased oxidative phosphorylation in both WT and KO using succinate and TMPD-ascorbate as complex II (b) and complex IV (c) substrates, respectively. Compared to time control, ISC–REP decreased the CRC in both WT and KO (d). However, the magnitude of the decrease in CRC in KO was less than that in WT (d), suggesting that elimination of CPNS1 inhibited MPTP opening after ischemia–reperfusion injury. Data are expressed as mean ± SD; *p < 0.05 vs. respective time control; ^†p < 0.05 vs. corresponding WT. N = 7 in each group.