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运动训练可能通过 DRP1 减少缺血再灌注心脏中的破碎线粒体。

Exercise training may reduce fragmented mitochondria in the ischemic-reperfused heart through DRP1.

机构信息

LAPEC UPR-4278, Avignon Université , Avignon, France.

UR407 INRAE Pathologie Végétale, INRAE , Avignon, France.

出版信息

J Gen Physiol. 2024 Dec 2;156(12). doi: 10.1085/jgp.202313485. Epub 2024 Nov 7.

DOI:10.1085/jgp.202313485
PMID:39508760
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11551008/
Abstract

Mitochondrial fission is a key trigger of cardiac ischemia-reperfusion injuries (IR). Exercise training is an efficient cardioprotective strategy, but its impact on mitochondrial fragmentation during IR remains unknown. Using isolated rat hearts, we found that exercise training limited the activation of dynamin-like protein 1 and limited mitochondrial fragmentation during IR. These results support the hypothesis that exercise training contributes to cardioprotection through its capacity to modulate the mitochondrial fragmentation during IR.

摘要

线粒体分裂是心脏缺血再灌注损伤（IR）的关键触发因素。运动训练是一种有效的心脏保护策略，但它对 IR 期间线粒体碎片化的影响尚不清楚。本研究使用分离的大鼠心脏，发现运动训练限制了动力相关蛋白 1 的激活，并限制了 IR 期间的线粒体碎片化。这些结果支持了运动训练通过调节 IR 期间的线粒体碎片化来促进心脏保护的假说。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d730/11551008/163dc004fe40/JGP_202313485_Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d730/11551008/dfdf429a1361/JGP_202313485_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d730/11551008/3a149c6ccc5b/JGP_202313485_Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d730/11551008/163dc004fe40/JGP_202313485_Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d730/11551008/dfdf429a1361/JGP_202313485_Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d730/11551008/3a149c6ccc5b/JGP_202313485_Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d730/11551008/163dc004fe40/JGP_202313485_Fig3.jpg

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本文引用的文献

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Hyperglycemia triggers RyR2-dependent alterations of mitochondrial calcium homeostasis in response to cardiac ischemia-reperfusion: Key role of DRP1 activation.高血糖触发 RyR2 依赖性改变线粒体钙动态平衡以应对心脏缺血再灌注：DRP1 激活的关键作用。
Redox Biol. 2024 Apr;70:103044. doi: 10.1016/j.redox.2024.103044. Epub 2024 Jan 19.
2
Mdivi-1 alleviates cardiac fibrosis post myocardial infarction at infarcted border zone, possibly via inhibition of Drp1-Activated mitochondrial fission and oxidative stress.Mdivi-1可减轻心肌梗死后梗死边缘区的心脏纤维化，可能是通过抑制Drp1激活的线粒体分裂和氧化应激来实现的。
Arch Biochem Biophys. 2022 Mar 30;718:109147. doi: 10.1016/j.abb.2022.109147. Epub 2022 Feb 7.
3
Increased protein S-nitrosylation in mitochondria: a key mechanism of exercise-induced cardioprotection.
线粒体中蛋白质 S-亚硝基化增加：运动诱导心脏保护的关键机制。
Basic Res Cardiol. 2021 Dec 23;116(1):66. doi: 10.1007/s00395-021-00906-3.
4
Emodin prevents renal ischemia-reperfusion injury via suppression of CAMKII/DRP1-mediated mitochondrial fission.大黄素通过抑制 CAMKII/DRP1 介导的线粒体分裂来预防肾缺血再灌注损伤。
Eur J Pharmacol. 2022 Feb 5;916:174603. doi: 10.1016/j.ejphar.2021.174603. Epub 2021 Nov 16.
5
The mitochondrial signaling peptide MOTS-c improves myocardial performance during exercise training in rats.线粒体信号肽 MOTS-c 可改善大鼠运动训练中心肌功能。
Sci Rep. 2021 Oct 11;11(1):20077. doi: 10.1038/s41598-021-99568-3.
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The cardiolipin-binding peptide elamipretide mitigates fragmentation of cristae networks following cardiac ischemia reperfusion in rats.心磷脂结合肽艾拉米肽可减轻大鼠心脏缺血再灌注后嵴网络的碎片化。
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7
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