内质网-线粒体互作在卒中后认知障碍中的研究进展

Research progress of the endoplasmic reticulum⁃mitochondrial interactions in post⁃stroke cognitive impairment

卒中后认知障碍(PSCI)指由卒中引起的一系列认知受损的临床综合征。尽管目前尚不清楚其具体的发病机制,但不少研究已证实内质网-线粒体间的交互串扰作为细胞内信号转导和物质代谢的关键枢纽,其调控的Ca^(2+)稳态、脂质代谢、线粒体动力学、自噬、神经炎症等多种生物学过程与PSCI的发生发展密切相关。因此,本文将对内质网-线粒体互作的生物学功能进行综述,并探讨其在PSCI中的具体作用,以发现新的治疗靶点,为今后PSCI靶向药物的开发提供新的理论依据和参考。

Post-stroke cognitive impairment(PSCI),refers to a range of clinical syndromes of cognitive impairment caused by stroke.Although its specific pathogenesis is still unclear,many studies have confirmed that endoplasmic reticulum-mitochondria interaction has become a key hub for intracellular signal transduction and substance metabolism,and its regulation of various biological processes,such as Ca^(2+)balance,lipid metabolism,mitochondrial dynamics,autophagy,and neuroinflammation,is closely related to the development of PSCI.There⁃fore,in this paper,we will review the various functions of endoplasmic reticulum-mitochondrial interactions and explore their specific roles in PSCI,in order to discover new therapeutic targets and provide new theoretical basis and references for the development of PSCI-targeted drugs in the future.