Mitochondrial clearance: mechanisms and roles in cellular fitness

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.

Keywords: adaptor; aging; autophagy; inflammation; mitochondria; neurodegeneration; ubiquitin.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aging* / genetics
  • Aging* / metabolism
  • Aging* / pathology
  • Animals
  • Autophagosomes* / genetics
  • Autophagosomes* / metabolism
  • Autophagosomes* / pathology
  • Autophagy / genetics*
  • Humans
  • Inflammation / genetics
  • Inflammation / metabolism
  • Mitochondria* / genetics
  • Mitochondria* / metabolism
  • Mitochondria* / pathology
  • Mitophagy / genetics*
  • Neurodegenerative Diseases* / genetics
  • Neurodegenerative Diseases* / metabolism
  • Neurodegenerative Diseases* / pathology
  • Reactive Oxygen Species / metabolism


  • Reactive Oxygen Species