Aging is a natural process in all living organisms defined as destruction of cell function as a result of long-term accumulation of damages. Autophagy is a cellular house safeguard pathway that is responsible for degrading damaged cellular organelles. Moreover, it maintains cellular homeostasis, controls lifetime and longevity. Damaged mitochondrial accumulation is a characteristic of aging that is associated with neurodegeneration. Mitochondria function as a principal energy source through supplying adenosine-5'-triphosphate (ATP) through oxidative phosphorylation that serves as fuel for neuronal function. Mitophagy and mitochondrial-specific autophagy play an important role in maintenance of neuronal health through the removal of dysfunctional and aged mitochondria. The mitochondrial quality control system involves different strategies for protecting against mitochondrial dysfunction and maintaining healthy mitochondria in cells. Mitochondrial function protection could be a strategy for the promotion of neuroprotection. Mitophagy could be an effective target for drug discovery. Therefore, further detailed studies for mechanism of mitophagy will advance our mitochondrial phenotype knowledge and understanding to disease pathogenesis. This review mainly focuses on aging-mediated mechanism of autophagy and mitophagy for maintaining the cellular homeostasis and longevity.
Keywords: aging; autophagy; cellular homeostasis; mitochondrial dysfunction; mitochondrial functioning mitophagy.