Abstract
Mitochondria are the crucial regulators for the major source of ATP for different cellular events. Due
to damage episodes, mitochondria have been established for a plethora ofalarming signals of stress that lead to
cellular deterioration, thereby causing programmed cell death. Defects in mitochondria play a key role in arbitrating
pathophysiological machinery with recent evince delineating a constructive role in mitophagy mediated mitochondrial
injury. Mitophagy has been known for the eradication of damaged mitochondria via the autophagy
process. Mitophagy has been investigated as an evolutionarily conserved mechanism for mitochondrial quality
control and homeostasis. Impaired mitophagy has been critically linked with the pathogenesis of inflammatory
diseases. Nevertheless, the exact mechanism is not quite revealed, and it is still debatable. The purpose of this
review was to investigate the possible role of mitophagy and its associated mechanism in inflammation-mediated
diseases at both the cellular and molecular levels.