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本文引用的文献

1
ST-segment elevation myocardial infarction.ST 段抬高型心肌梗死。
Nat Rev Dis Primers. 2019 Jun 6;5(1):39. doi: 10.1038/s41572-019-0090-3.
2
Propofol Ameliorates H9c2 Cells Apoptosis Induced by Oxygen Glucose Deprivation and Reperfusion Injury via Inhibiting High Levels of Mitochondrial Fusion and Fission.丙泊酚通过抑制高水平的线粒体融合与分裂改善氧糖剥夺和再灌注损伤诱导的H9c2细胞凋亡。
Front Pharmacol. 2019 Feb 12;10:61. doi: 10.3389/fphar.2019.00061. eCollection 2019.
3
Evolving Concepts of Mitochondrial Dynamics.线粒体动态的演变概念。
Annu Rev Physiol. 2019 Feb 10;81:1-17. doi: 10.1146/annurev-physiol-020518-114358. Epub 2018 Sep 26.
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Mitochondrial dynamics: overview of molecular mechanisms.线粒体动力学：分子机制概述。
Essays Biochem. 2018 Jul 20;62(3):341-360. doi: 10.1042/EBC20170104.
5
Novel insights into the role of mitochondrial fusion and fission in cardiomyocyte apoptosis induced by ischemia/reperfusion.线粒体融合和裂变在缺血/再灌注诱导的心肌细胞凋亡中的作用的新见解。
J Cell Physiol. 2018 Aug;233(8):5589-5597. doi: 10.1002/jcp.26522. Epub 2018 Mar 12.
6
ALDH2 protects against alcoholic cardiomyopathy through a mechanism involving the p38 MAPK/CREB pathway and local renin-angiotensin system inhibition in cardiomyocytes.ALDH2 通过一种涉及心肌细胞中 p38 MAPK/CREB 通路和局部肾素-血管紧张素系统抑制的机制来预防酒精性心肌病。
Int J Cardiol. 2018 Apr 15;257:150-159. doi: 10.1016/j.ijcard.2017.11.094.
7
Targeting ALDH2 for Therapeutic Interventions in Chronic Pain-Related Myocardial Ischemic Susceptibility.针对慢性疼痛相关心肌缺血易感性的 ALDH2 靶向治疗干预。
Theranostics. 2018 Jan 1;8(4):1027-1041. doi: 10.7150/thno.22414. eCollection 2018.
8
Roles of mitochondrial dynamics modulators in cardiac ischaemia/reperfusion injury.线粒体动态调节剂在心肌缺血/再灌注损伤中的作用。
J Cell Mol Med. 2017 Nov;21(11):2643-2653. doi: 10.1111/jcmm.13330. Epub 2017 Sep 22.
9
The constriction and scission machineries involved in mitochondrial fission.参与线粒体分裂的收缩和断裂机制。
J Cell Sci. 2017 Sep 15;130(18):2953-2960. doi: 10.1242/jcs.199562. Epub 2017 Aug 25.
10
Mdivi-1 induced acute changes in the angiogenic profile after ischemia-reperfusion injury in female mice.Mdivi-1在雌性小鼠缺血再灌注损伤后诱导血管生成谱急性变化。
Physiol Rep. 2017 Jun;5(11). doi: 10.14814/phy2.13298.

乙醛脱氢酶2可维持线粒体形态并减轻缺氧/复氧诱导的心肌细胞损伤。

Aldehyde dehydrogenase 2 preserves mitochondrial morphology and attenuates hypoxia/reoxygenation-induced cardiomyocyte injury.

作者信息

Zhang Rui, Xue Meng-Yang, Liu Bao-Shan, Wang Wen-Jun, Fan Xin-Hui, Zheng Bo-Yuan, Yuan Qiu-Huan, Xu Feng, Wang Jia-Li, Chen Yu-Guo

机构信息

Department of Emergency Medicine and Chest Pain Center, Qilu Hospital, Shandong University, Jinan, China.

Shandong Provincal Clinical Research Center for Emergency and Critical Care Medicine of Shandong Province, Institute of Emergency and Critical Care Medicine of Shandong University, Qilu Hospital, Shandong University, Jinan, China.

出版信息

World J Emerg Med. 2020;11(4):246-254. doi: 10.5847/wjem.j.1920-8642.2020.04.007.

DOI:10.5847/wjem.j.1920-8642.2020.04.007
PMID:33014221
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7517403/
Abstract

BACKGROUND

Disturbance of mitochondrial fission and fusion (termed mitochondrial dynamics) is one of the leading causes of ischemia/reperfusion (I/R)-induced myocardial injury. Previous studies showed that mitochondrial aldehyde dehydrogenase 2 (ALDH2) conferred cardioprotective effect against myocardial I/R injury and suppressed I/R-induced excessive mitophagy in cardiomyocytes. However, whether ALDH2 participates in the regulation of mitochondrial dynamics during myocardial I/R injury remains unknown.

METHODS

In the present study, we investigated the effect of ALDH2 on mitochondrial dynamics and the underlying mechanisms using the H9c2 cells exposed to hypoxia/reoxygenation (H/R) as an model of myocardial I/R injury.

RESULTS

Cardiomyocyte apoptosis was significantly increased after oxygen-glucose deprivation and reoxygenation (OGD/R), and ALDH2 activation largely decreased the cardiomyocyte apoptosis. Additionally, we found that both ALDH2 activation and overexpression significantly inhibited the increased mitochondrial fission after OGD/R. Furthermore, we found that ALDH2 dominantly suppressed dynamin-related protein 1 (Drp1) phosphorylation (Ser616) and adenosine monophosphate-activated protein kinase (AMPK) phosphorylation (Thr172) but not interfered with the expression levels of mitochondrial shaping proteins.

CONCLUSIONS

We demonstrate the protective effect of ALDH2 against cardiomyocyte H/R injury with a novel mechanism on mitochondrial fission/fusion.

摘要

背景

线粒体分裂与融合紊乱（称为线粒体动力学）是缺血/再灌注（I/R）诱导的心肌损伤的主要原因之一。先前的研究表明，线粒体醛脱氢酶2（ALDH2）对心肌I/R损伤具有心脏保护作用，并抑制I/R诱导的心肌细胞过度线粒体自噬。然而，ALDH2是否参与心肌I/R损伤期间线粒体动力学的调节仍不清楚。

方法

在本研究中，我们以暴露于缺氧/复氧（H/R）的H9c2细胞作为心肌I/R损伤模型，研究了ALDH2对线粒体动力学的影响及其潜在机制。

结果

氧糖剥夺和复氧（OGD/R）后心肌细胞凋亡显著增加，而ALDH2激活可大大降低心肌细胞凋亡。此外，我们发现ALDH2激活和过表达均显著抑制OGD/R后增加的线粒体分裂。此外，我们发现ALDH2主要抑制动力相关蛋白1（Drp1）磷酸化（Ser616）和腺苷单磷酸激活蛋白激酶（AMPK）磷酸化（Thr172），但不干扰线粒体形态蛋白的表达水平。

结论

我们证明了ALDH2通过一种关于线粒体分裂/融合的新机制对心肌细胞H/R损伤具有保护作用。