Alda-1 treatment promotes the therapeutic effect of mitochondrial transplantation for myocardial ischemia-reperfusion injury

移植 ALDH2 线粒体 再灌注损伤 线粒体通透性转换孔 缺氧(环境) 缺血 医学 化学 药理学 细胞生物学 细胞凋亡 生物 心脏病学 内科学 程序性细胞死亡 生物化学 醛脱氢酶 氧气 有机化学
作者
Xiaolei Sun,Rifeng Gao,Wenjia Li,Yongchao Zhao,Heng Yang,Hang Chen,Hao Jiang,Zhen Dong,Jingjing Hu,Jin Liu,Yunzeng Zou,Aijun Sun,Junbo Ge
出处
期刊:Bioactive Materials [Elsevier]
卷期号:6 (7): 2058-2069 被引量:52
标识
DOI:10.1016/j.bioactmat.2020.12.024
摘要

Mitochondrial damage is a critical driver in myocardial ischemia-reperfusion (I/R) injury and can be alleviated via the mitochondrial transplantation. The efficiency of mitochondrial transplantation is determined by mitochondrial vitality. Because aldehyde dehydrogenase 2 (ALDH2) has a key role in regulating mitochondrial homeostasis, we aimed to investigate its potential therapeutic effects on mitochondrial transplantation via the use of ALDH2 activator, Alda-1. Our present study demonstrated that time-dependent internalization of exogenous mitochondria by cardiomyocytes along with ATP production were significantly increased in response to mitochondrial transplantation. Furthermore, Alda-1 treatment remarkably promoted the oxygen consumption rate and baseline mechanical function of cardiomyocytes caused by mitochondrial transplantation. Mitochondrial transplantation inhibited cardiomyocyte apoptosis induced by the hypoxia-reoxygenation exposure, independent of Alda-1 treatment. However, promotion of the mechanical function of cardiomyocytes exposed to hypoxia-reoxygenation treatment was only observed after mitochondrial Alda-1 treatment and transplantation. By using a myocardial I/R mouse model, our results revealed that transplantation of Alda-1-treated mitochondria into mouse myocardial tissues limited the infarction size after I/R injury, which was at least in part due to increased mitochondrial potential-mediated fusion. In conclusion, ALDH2 activation in mitochondrial transplantation shows great potential for the treatment of myocardial I/R injury.
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