Stroke Renaissance Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan and Core Research for Evolutionary Medical Science and Technology (CREST), Japan Agency for Medical Research and Development (AMED), Tokyo 100-0004, Japan; Division of Biochemistry, Faculty of Pharmacy, Keio University, Tokyo 105-8512, Japan.
Stroke Renaissance Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan and Core Research for Evolutionary Medical Science and Technology (CREST), Japan Agency for Medical Research and Development (AMED), Tokyo 100-0004, Japan.
Neurosci Res. 2023 Feb;187:67-71. doi: 10.1016/j.neures.2022.10.002. Epub 2022 Oct 4.
Stroke is a leading cause of death and disability worldwide, but there are a limited number of therapies that improve patients' functional recovery. The complicated mechanisms of post-stroke neuroinflammation, which is responsible for secondary ischemic neuronal damage, have been clarified by extensive research. Activation of microglia and astrocytes due to ischemic insults is implicated in the production of pro-inflammatory factors, formation of the glial scar, and breakdown of the blood-brain barrier. This leads to the infiltration of leukocytes, which are activated by damage-associated molecular patterns (DAMPs) to produce pro-inflammatory factors and induce additional neuronal damage. In this review, we focus on the glial mechanisms underlying sterile post-ischemic inflammation after stroke.
中风是全球范围内导致死亡和残疾的主要原因，但能够改善患者功能恢复的治疗方法却十分有限。通过广泛的研究，已经阐明了中风后神经炎症的复杂机制，它是导致继发性缺血性神经元损伤的原因。缺血性损伤导致小胶质细胞和星形胶质细胞的激活，进而产生促炎因子、形成胶质瘢痕，并破坏血脑屏障。这导致白细胞浸润，而损伤相关分子模式（DAMPs）会激活白细胞，使其产生促炎因子并引发额外的神经元损伤。在这篇综述中，我们重点介绍中风后无菌性缺血后炎症的神经胶质机制。
