Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China; Department of Emergency, Xuanwu Hospital, Capital Medical University, Beijing, China.
Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China; Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China.
Neurobiol Dis. 2023 Aug;184:106200. doi: 10.1016/j.nbd.2023.106200. Epub 2023 Jun 13.
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.
少突胶质细胞(OLs)是中枢神经系统形成髓鞘的细胞,对轴突的完整性和功能至关重要。缺氧缺血发作可通过兴奋性毒性、氧化应激、炎症和线粒体功能障碍对这些脆弱的细胞造成严重损伤,导致轴突萎缩、神经元功能障碍和神经功能障碍。OLs 的损伤会导致脱髓鞘和髓鞘形成障碍,严重影响轴突的功能、结构、代谢和存活。成人中风、脑室周围白质软化和中风后认知障碍主要针对 OLs,使其成为一个关键的治疗靶点。针对 OLs、髓鞘及其受体的治疗策略应该得到更多的重视,以减轻缺血损伤,并在中风后建立功能恢复。本综述总结了 OLs 在缺血性损伤中的功能的最新进展,以及目前和新兴的原则,这些原则为保护 OLs 免受死亡的策略提供了基础。