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Aldehyde dehydrogenase 2 preserves mitochondrial morphology and attenuates hypoxia/reoxygenationinduced cardiomyocyte injury

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World Journal of Emergency Medicine 2020年第4期11卷 246-254页

作者： Rui Zhang Meng-yang Xue Bao-shan Liu Wen-jun Wang Xin-hui Fan Bo-yuan Zheng Qiu-huan Yuan Feng Xu Jia-li Wang Yu-guo Chen Department of Emergency Medicine and Chest Pain Center Qilu HospitalShandong UniversityJinanChina Shandong Provincal Clinical Research Center for Emergency and Critical Care Medicine of Shandong Province Institute of Emergency and Critical Care Medicine of Shandong UniversityQilu HospitalShandong UniversityJinanChina Key Laboratory of Emergency and Critical Care Medicine of Shandong Province Key Laboratory of Cardiopulmonary-Cerebral Resuscitation Research of Shandong ProvinceQilu HospitalShandong UniversityJinanChina The Key Laboratory of Cardiovascular Remodeling and Function Research Chinese Ministry of EducationChinese Ministry of Health and Chinese Academy of Medical Sciencesthe State and Shandong Province Joint Key Laboratory of Translational Cardiovascular MedicineQilu HospitalShandong UniversityJinanChina

BACKGROUND:Disturbance of mitochondrial fi ssion 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 in vitro 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.

关键词： myocardial hypoxia/reoxygenation injury Aldehyde dehydrogenase 2 Mitochondrial fi ssion/fusion Mitochondrial dynamics Dynamin-related protein 1

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