《生命科学》 2025, 37(2): 109-117

线粒体功能障碍在慢性脑低灌注介导的血管性认知障碍中的作用

刘竹暄^1,2 , 曾珊珊² , 谭惠中^1,2 , 张秀丽³ , 伍大华^2,*

¹湖南中医药大学研究生院，长沙 410208 ²湖南省中医药研究院附属医院 脑病科，长沙 410006 ³湖南中医药大学科技创新中心，长沙 410208

摘　要：

线粒体作为真核生物细胞的能量工厂与氧化中心，对于维持大脑的正常运转至关重要，其功能障碍与血管性认知障碍(vascular cognitive impairment, VCI) 病理机制之间存在不可忽视的联系。VCI 最常见的潜在病因是慢性脑低灌注(chronic cerebral hypoperfusion, CCH)，其通过引发长期的能量与离子稳态失衡、氧化应激和神经炎症，造成神经元死亡、突触功能障碍、血脑屏障破坏以及白质损伤等连锁反应。目前，线粒体功能障碍与上述病理事件之间的关系仍不明确。本文意在梳理CCH 引发VCI 的病理机制，并重点讨论线粒体功能障碍如何参与其中，以期更好地厘清缺血性脑病中线粒体损伤与保护的作用，为靶向线粒体功能修复以开发新型VCI 治疗干预措施提供新的观点。

通讯作者：伍大华 , Email:893049352@qq.com

The role of mitochondrial dysfunction in vascular cognitive impairment mediated by chronic cerebral hypoperfusion

LIU Zhu-Xuan^1,2 , ZENG Shan-Shan² , TAN Hui-Zhong^1,2 , ZHANG Xiu-Li³ , WU Da-Hua^2,*

¹Graduate School, Hunan University of Chinese Medicine, Changsha 410208, China ²Department of Neurology, Affiliated Hospital of Hunan Provincial Academy of Chinese Medicine, Changsha 410006, China ³Science and Technology Innovation Center, Hunan University of Chinese Medicine, Changsha 410208, China

Abstract:

Mitochondria as the energy factory and oxidation center of eukaryotic cells are essential for maintaining the normal functioning of the brain. The complex links of mitochondrial dysfunction to vascular cognitive impairment (VCI) cannot be overlooked. The most common underlying cause of VCI is chronic cerebral hypoperfusion (CCH), which triggers long-term imbalance of energy and ion homeostasis, oxidative stress and neuroinflammation, resulting in a series of consequences, including neuronal death, synaptic dysfunction, bloodbrain barrier disruption and white matter damage. However, the relationship between mitochondrial dysfunction and the above pathological events is not fully understood. This article aims to sort out the pathological mechanism of VCI induced by CCH and emphasize the key role of mitochondrial dysfunction in this process, in order to better clarify the role of mitochondrial damage and protection in ischemic encephalopathy and provide new insights into the developing novel therapeutic interventions for VCI by targeted mitochondrial function repair.

Communication Author：WU Da-Hua , Email:893049352@qq.com