Mitophagy is the selective degradation of mitochondria by autophagy Mitochondria are essential organelles that regulate cellular energy homeostasis and cell death It often occurs to defective mitochondria following damage or stress
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The process of mitophagy was first described in 1915 by margaret reed lewis and warren harmon lewis
线粒体自噬 (Mitochondrial autophagy, mitophagy) 作为一种重要线粒体质量控制机制，在活性氧 (ROS) 胁迫等应激作用下，会导致线粒体 DNA (Mitochondrial DNA, mtDNA) 突变逐渐累积，还会使细胞内线粒体膜电位降低和去极化损伤，并最终导致细胞死亡 [1] [2]。
Here, we summarize the signaling pathways and mechanisms that regulate mitophagy Furthermore, we discuss how alterations in mitophagy affect mitochondrial homeostasis and disease development. Explore the mitophagy pathways like pink1/parkin, its role in disease, and the tools available to detect mitophagy in research and diagnostics. In this review, we describe the basic mechanisms of mitophagy and how mitophagy can be assessed in human blood, the immune system and tissues, including muscle, brain and liver.
Mitophagy is a quality control pathway that targets dysfunctional mitochondria for degradation It does so by sequestering damaged mitochondria within double membrane structures termed autophagosomes before delivering them to the acidic and proteolytic environment of lysosomes [1, 2, 3, 4, 5]. 线粒体自噬（Mitophagy）是真核细胞通过自噬机制选择性清除功能失调或者多余线粒体的一种高度保守的细胞进程，该过程能很好地调整线粒体数目并维持细胞能量代谢的稳定。 Mitophagy removes and recycles damaged mitochondria and regulates the biogenesis of new, fully functional ones preserving healthy mitochondrial functions and activities.
Here, we review our current molecular understanding of mitophagy, and its physiological implications, and discuss how multiple mitophagy pathways coordinately modulate mitochondrial fitness and populations.
