Majumder Dhriti
Alliance University, Bengaluru, Karnataka, India.
Neurosci Insights. 2024 Oct 22;19:26331055241292600. doi: 10.1177/26331055241292600. eCollection 2024.
Stroke remains a leading cause of mortality and disability, with ischemic stroke being the most common type. It occurs due to reduced cerebral blood flow, leading to a cascade of events initiated by oxygen and nutrient deprivation, triggering excitotoxicity, oxidative stress, and inflammation and finally culminating in neuronal injury and death. Key molecular players in ischemic stroke include glutamate receptors, acid-sensing ion channels, and purinergic receptors, exacerbating cellular damage through calcium influx, oxidative stress, and mitochondrial dysfunction. Understanding these mechanisms has shaped therapeutic strategies, such as neuroprotective agents and stem cell therapies. Current treatments such as tissue plasminogen activator (tPA) emphasize timely intervention, yet challenges persist in patient-specific variability and accessibility. This review provides an overview of ischemic stroke pathophysiology, emphasizing cellular responses to ischemia and current and future therapeutic approaches including stem cell therapies aimed at mitigating stroke-induced disabilities and improving long-term outcomes.
中风仍然是导致死亡和残疾的主要原因，其中缺血性中风是最常见的类型。它是由于脑血流量减少而发生的，导致一系列由氧和营养物质剥夺引发的事件，引发兴奋性毒性、氧化应激和炎症，最终导致神经元损伤和死亡。缺血性中风的关键分子参与者包括谷氨酸受体、酸敏感离子通道和嘌呤能受体，它们通过钙内流、氧化应激和线粒体功能障碍加剧细胞损伤。对这些机制的理解塑造了治疗策略，如神经保护剂和干细胞疗法。目前的治疗方法，如组织纤溶酶原激活剂（tPA），强调及时干预，但在患者个体差异和可及性方面仍然存在挑战。本综述概述了缺血性中风的病理生理学，强调细胞对缺血的反应以及当前和未来的治疗方法，包括旨在减轻中风所致残疾和改善长期预后的干细胞疗法。
