线粒体自噬与衰老

Mitophagy and aging

线粒体是三羧酸循环的主要场所,几乎是所有真核细胞的能量供应站。衰老伴随着线粒体功能的丧失和损伤线粒体的累积。线粒体自噬是细胞清除衰老损伤线粒体的主要机制。细胞内的线粒体自噬不足,损伤线粒体的累积可以作为细胞衰老的标志物。因此,研究线粒体自噬的机制、调控途径以及寻找干预线粒体自噬的策略,对于延缓衰老具有重要意义。该文阐述了线粒体自噬与衰老相关的分子调控网络以及干预线粒体自噬延缓衰老的策略及研究方向,旨在推进靶向线粒体自噬治疗衰老相关疾病的发展。

Mitochondria is the central hub of the tricarboxylic acid cycle and plays a crucial role in generating cellular energy and as the primary energy providers for almost all eukaryotic cells.The aging process is characterized by a decline in mitochondrial function and the accumulation of damaged mitochondria.Mitophagy serves as the primary mechanism through which cells eliminate aging-related damaged mitochondria.Inadequate mitochondrial autophagy and the accumulation of damaged mitochondria can be indicative of the aging process.Therefore,investigating the mechanisms and regulatory pathways of mitophagy and identifying strategies to modulate this process are of paramount importance in delaying the aging process.This review provides a comprehensive overview of the molecular regulatory networks connecting mitophagy and aging,as well as discusses strategies to manipulate mitophagy for the purpose of delaying the aging process.Additionally,this review explores future prospects in this field.The aim is to advance the development of targeted mitochondrial autophagy for the treatment of age-related diseases.