线粒体自噬与血管性认知障碍的相关性研究进展

Research Progress on the Correlation Between Mitophagy and Vascular Cognitive Impairment

  • 摘要: 血管性认知障碍是由脑血管问题导致的认知功能受损,严重影响老年人生活质量,但缺乏有效治疗方法。线粒体自噬是一种线粒体自我清除机制,是近年来神经系统疾病研究的热点机制。大量研究表明,线粒体自噬能够调节氧化应激、神经炎症,影响神经元凋亡,其相关信号通路,如PINK/Parkin、BNIP3/Nip和FUNDC1受体、PI3K/Akt/mTOR以及AMPK通路,已成为治疗血管性认知障碍的潜在靶点。本文围绕线粒体自噬在血管性认知障碍中的作用机制以及潜在治疗策略进行阐述,以期为临床治疗提供新思路。

     

    Abstract: Vascular cognitive impairment (VCI), caused by cerebrovascular dysfunction, severely impacts the quality of life in the elderly population, yet effective therapeutic approaches remain limited. Mitophagy, a selective mitochondrial quality-control mechanism, has emerged as a critical focus in neurological disease research. Accumulating evidence indicates that mitophagy modulates oxidative stress, neuroinflammation, and neuronal apoptosis. Key signaling pathways associated with mitophagy—including PINK1/Parkin, BNIP3/Nix, FUNDC1, PI3K/Akt/mTOR, and AMPK—have been identified as potential therapeutic targets for VCI. This review summarizes the mechanistic roles of mitophagy in VCI pathogenesis and explores emerging therapeutic strategies targeting these pathways, aiming to provide novel insights for clinical intervention and advance the development of effective treatments for VCI.

     

/

返回文章
返回