线粒体
缺血
线粒体分裂
氧化应激
神经科学
线粒体融合
再灌注损伤
生物
医学
细胞生物学
线粒体DNA
内科学
内分泌学
生物化学
基因
作者
Jie Huang,Lei Chen,Zi‐Meng Yao,Xiao‐Rong Sun,Xuhui Tong,Shuying Dong
标识
DOI:10.1016/j.biopha.2023.114671
摘要
Stroke is one of the leading causes of death and long-term disability worldwide. More than 80 % of strokes are ischemic, caused by an occlusion of cerebral arteries. Without question, restoration of blood supply as soon as possible is the first therapeutic strategy. Nonetheless paradoxically, reperfusion can further aggravate the injury through a series of reactions known as cerebral ischemia-reperfusion injury (CIRI). Mitochondria play a vital role in promoting nerve survival and neurological function recovery and mitochondrial dysfunction is considered one of the characteristics of CIRI. Neurons often die due to oxidative stress and an imbalance in energy metabolism following CIRI, and there is a strong association with mitochondrial dysfunction. Altered mitochondrial dynamics is the first reaction of mitochondrial stress. Mitochondrial dynamics refers to the maintenance of the integrity, distribution, and size of mitochondria as well as their ability to resist external stimuli through a continuous cycle of mitochondrial fission and fusion. Therefore, improving mitochondrial dynamics is a vital means of treating CIRI. This review discusses the relationship between mitochondria and CIRI and emphasizes improving mitochondrial dynamics as a potential therapeutic approach to improve the prognosis of CIRI.
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