Stroke is one of the main causes of mortality and disability in most countries of the world. The only way of managing patients with ischemic stroke is the use of intravenous tissue plasminogen activator and endovascular thrombectomy. However, very few patients receive these treatments as the therapeutic time window is narrow after an ischemic stroke. The paucity of stroke management approaches can only be addressed by identifying new possible therapeutic targets. Mitochondria have been a rare target in the clinical management of stroke. Previous studies have only investigated the bioenergetics and apoptotic roles of this organelle; however, the mitochondrion is now considered as a key organelle that participates in many cellular and molecular functions. This review discusses the mitochondrial mechanisms in cerebral ischemia such as its role in reactive oxygen species (ROS) generation, apoptosis, and electron transport chain dysfunction. Understanding the mechanisms of mitochondria in neural cell death during ischemic stroke might help to design new therapeutic targets for ischemic stroke as well as other neurological diseases.

中文翻译：

---

缺血性中风和线粒体：机制和目标

中风是世界上大多数国家死亡和残疾的主要原因之一。治疗缺血性中风患者的唯一方法是使用静脉内组织纤溶酶原激活剂和血管内血栓切除术。然而，很少有患者接受这些治疗，因为缺血性中风后的治疗时间窗口很窄。中风管理方法的缺乏只能通过确定新的可能的治疗目标来解决。线粒体一直是中风临床管理中的一个罕见目标。以前的研究只研究了这种细胞器的生物能量学和凋亡作用；然而，线粒体现在被认为是参与许多细胞和分子功能的关键细胞器。本综述讨论了脑缺血的线粒体机制，例如其在活性氧 (ROS) 生成、细胞凋亡和电子传递链功能障碍中的作用。了解线粒体在缺血性中风期间神经细胞死亡的机制可能有助于为缺血性中风和其他神经系统疾病设计新的治疗靶点。