首页|期刊导航|中国比较医学杂志|基于"虚气留滞"理论探讨线粒体自噬对缺血性脑卒中的调控机制

基于"虚气留滞"理论探讨线粒体自噬对缺血性脑卒中的调控机制OA

Exploring the regulatory mechanism of mitophagy on ischemic stroke based on the theory of"Qi Deficiency and Stasis"

中文摘要英文摘要

缺血性脑卒中(IS)是常见的脑血管疾病,其病机复杂且病程较长,缠绵难愈.在中医"虚气留滞"理论指导下,可将其概括为"虚气"为本、"留滞"为标的本虚标实之证,现代研究发现,线粒体自噬作为维持细胞稳态的关键环节,广泛参与到IS的调控之中,其功能状态与"虚气留滞"病机变化相关,故本文基于中医"虚气留滞"理论,系统探讨其与线粒体自噬在IS发生发展中的内在联系并提供治疗策略,通过构建中医病机与现代生物学机制的对话桥梁,以期为从"虚气留滞"理论靶向线粒体自噬防治IS提供新的理论依据和研究思路.

Ischemic stroke(IS)is a common cerebrovascular disease with a complex pathogenesis and a prolonged,refractory clinical course.Under the guidance of the traditional Chinese medicine theory of"Qi Deficiency and Stasis,"IS can be characterized as a syndrome of deficiency in origin and excess in manifestation,with"Qi Deficiency"as the root and"Stasis"as the manifestation.Recent research has demonstrated the extensive involvement of mitophagy,as a key process in maintaining cellular homeostasis,in the regulation of IS.Its functional state aligns with the pathological changes described in the"Qi Deficiency and Stasis"theory.This review systematically explores the intrinsic relationship between the"Qi Deficiency and Stasis"theory and mitophagy in the occurrence and progression of IS,while proposing therapeutic strategies.By establishing a bridge between traditional Chinese medicine pathogenesis and modern biological mechanisms,it provides a new theoretical basis and research direction for targeting mitophagy in the prevention and treatment of IS based on the"Qi Deficiency and Stasis"theory.

杭雪莹;郝颖煦;刘向哲

河南中医药大学第一附属医院脑病中心,郑州 450046||河南中医药大学第一临床医学院,郑州 450046河南中医药大学第一附属医院脑病中心,郑州 450046||河南中医药大学第一临床医学院,郑州 450046河南中医药大学第一附属医院脑病中心,郑州 450046||中西医防治重大疾病河南省协同创新中心,郑州 450046

医药卫生

虚气留滞缺血性脑卒中线粒体自噬中医药

Qi Deficiency and Stasisischemic strokemitophagytraditional Chinese medicine

《中国比较医学杂志》 2026 (9)

131-142,12

国家重点研发计划资助项目(2022YFC3501103)河南省科技攻关项目(242102311277)河南省"双一流"创建学科中医学科研专项课题(HSRP-DFCTCM-2023-2-18)河南省中医药传承与创新人才工程(仲景工程)中医药学科领军人才(豫卫中医函[2021]8号)河南省卫健委国家中医药传承创新中心联合共建科研重大专项(2024ZXZX1017).

10.3969/j.issn.1671-7856.2026.09.011

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