兴奋毒性
神经科学
冲程(发动机)
医学
少突胶质细胞
髓鞘
缺血
室周白质软化
缺氧(环境)
神经保护
谷氨酸受体
中枢神经系统
生物
受体
内科学
有机化学
化学
氧气
工程类
胎龄
怀孕
机械工程
遗传学
作者
Shuangfeng Huang,Changhong Ren,Yumin Luo,Yuchuan Ding,Xunming Ji,Sijie Li
标识
DOI:10.1016/j.nbd.2023.106200
摘要
Oligodendrocytes (OLs), the myelin-forming cells of the central nervous system, are integral to axonal integrity and function. Hypoxia-ischemia episodes can cause severe damage to these vulnerable cells through excitotoxicity, oxidative stress, inflammation, and mitochondrial dysfunction, leading to axonal dystrophy, neuronal dysfunction, and neurological impairments. OLs damage can result in demyelination and myelination disorders, severely impacting axonal function, structure, metabolism, and survival. Adult-onset stroke, periventricular leukomalacia, and post-stroke cognitive impairment primarily target OLs, making them a critical therapeutic target. Therapeutic strategies targeting OLs, myelin, and their receptors should be given more emphasis to attenuate ischemia injury and establish functional recovery after stroke. This review summarizes recent advances on the function of OLs in ischemic injury, as well as the present and emerging principles that serve as the foundation for protective strategies against OLs deaths.
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