Laboratory of Mitochondrial Dynamics, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan.
FEBS Lett. 2021 Apr;595(8):1239-1263. doi: 10.1002/1873-3468.14060. Epub 2021 Mar 8.
Mitophagy is one of the selective autophagy pathways that catabolizes dysfunctional or superfluous mitochondria. Under mitophagy-inducing conditions, mitochondria are labeled with specific molecular landmarks that recruit the autophagy machinery to the surface of mitochondria, enclosed into autophagosomes, and delivered to lysosomes (vacuoles in yeast) for degradation. As damaged mitochondria are the major sources of reactive oxygen species, mitophagy is critical for mitochondrial quality control and cellular health. Moreover, appropriate control of mitochondrial quantity via mitophagy is vital for the energy supply-demand balance in cells and whole organisms, cell differentiation, and developmental programs. Thus, it seems conceivable that defects in mitophagy could elicit pleiotropic pathologies such as excess inflammation, tissue injury, neurodegeneration, and aging. In this review, we will focus on the molecular basis and physiological relevance of mitophagy, and potential of mitophagy as a therapeutic target to overcome such disorders.
自噬是一种选择性自噬途径，可分解功能失调或多余的线粒体。在诱导自噬的条件下，线粒体被特定的分子标记物标记，这些标记物招募自噬机制到线粒体表面，被包裹在自噬体中，并被递送至溶酶体（酵母中的液泡）进行降解。由于受损的线粒体是活性氧的主要来源，因此自噬对于线粒体的质量控制和细胞健康至关重要。此外，通过自噬适当控制线粒体的数量对于细胞和整个生物体的能量供应需求平衡、细胞分化和发育程序都至关重要。因此，可以想象，自噬缺陷可能会引发多种病理，如过度炎症、组织损伤、神经退行性变和衰老。在这篇综述中，我们将重点介绍自噬的分子基础和生理相关性，以及自噬作为治疗靶点以克服这些疾病的潜力。
