Open AccessAldehyde dehydrogenase 2 preserves mitochondrial morphology and attenuates hypoxia/reoxygenation-induced cardiomyocyte injury
Author(s) -
Rui Zhang,
Mengyang Xue,
Baoshan Liu,
Wenjun Wang,
Xiaoran Fan,
Boyuan Zheng,
Qiuhuan Yuan,
Feng Xu,
Jiali Wang,
Yuguo Chen
Publication year - 2020
Publication title -
world journal of emergency medicine
Language(s) - English
Resource type - Journals
ISSN - 1920-8642
DOI - 10.5847/wjem.j.1920-8642.2020.04.007
Subject(s) - aldh2 , mitochondrial fission , dnm1l , mitochondrion , microbiology and biotechnology , hypoxia (environmental) , ampk , mitophagy , apoptosis , reactive oxygen species , protein kinase a , medicine , reperfusion injury , phosphorylation , biology , ischemia , chemistry , biochemistry , aldehyde dehydrogenase , oxygen , enzyme , organic chemistry , autophagy
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.