Mitochondria, the ‘powerhouse’ of eukaryotic cells, play a key role in cellular homeostasis. However, defective mitochondria increase mitochondrial ROS (mtROS) production and cell-free mitochondrial DNA (mtDNA) release, leading to increased inflammation. Mitophagy is a vital pathway, which selectively removes defective mitochondria through the process of autophagy. Thus, an impairment in the mitophagy pathway might trigger the gradual accumulation of defective mitochondria. Accumulating evidence suggest that inflammation and mitochondrial dysfunction are linked to the pathogenesis of depression. In this article, we have reviewed the role of impaired mitophagy as a contributing factor in depression pathophysiology. Further, we have discussed the potential therapeutic interventions aimed at modulating mitophagy in depression.

线粒体是真核细胞的“动力源”，在细胞稳态中发挥着关键作用。然而，有缺陷的线粒体会增加线粒体 ROS (mtROS) 的产生和无细胞线粒体 DNA (mtDNA) 的释放，从而导致炎症增加。线粒体自噬是一种重要的途径，它通过自噬过程选择性地去除有缺陷的线粒体。因此，线粒体自噬途径的损伤可能会引发缺陷线粒体的逐渐积累。越来越多的证据表明炎症和线粒体功能障碍与抑郁症的发病机制有关。在本文中，我们回顾了线粒体自噬受损在抑郁症病理生理学中的作用。此外，我们讨论了旨在调节抑郁症线粒体自噬的潜在治疗干预措施。