Department of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
Laboratory of Neurological Diseases and Brain Function, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
Oxid Med Cell Longev. 2022 Apr 28;2022:3335887. doi: 10.1155/2022/3335887. eCollection 2022.
In ischemic stroke (IS), accumulation of the misfolded proteins in the endoplasmic reticulum (ER) and mitochondria-induced oxidative stress (OS) has been identified as the indispensable inducers of secondary brain injury. With the increasing recognition of an association between ER stress and OS with ischemic stroke and with the improved understanding of the underlying molecular mechanism, novel targets for drug therapy and new strategies for therapeutic interventions are surfacing. This review discusses the molecular mechanism underlying ER stress and OS response as both causes and consequences of ischemic stroke. We also summarize the latest advances in understanding the importance of ER stress and OS in the pathogenesis of ischemic stroke and discuss potential strategies and clinical trials explicitly aiming to restore mitochondria and ER dynamics after IS.
在缺血性脑卒中(IS)中,内质网(ER)中错误折叠蛋白的积累和线粒体诱导的氧化应激(OS)已被确定为继发性脑损伤的不可或缺的诱导因素。随着人们对 ER 应激和 OS 与缺血性脑卒中之间的关联的认识不断提高,以及对潜在分子机制的理解不断深入,新的药物治疗靶点和治疗干预新策略不断涌现。本综述讨论了 ER 应激和 OS 反应的分子机制,它们既是缺血性脑卒中的原因,也是其后果。我们还总结了在缺血性脑卒中发病机制中理解 ER 应激和 OS 重要性的最新进展,并讨论了明确旨在恢复 IS 后线粒体和 ER 动力学的潜在策略和临床试验。