The Roles of Autophagy in Oxidative Stress

Autophagy is an evolutionarily conserved, lysosome-dependent, intracellular degradation process that is essential for maintaining cellular homeostasis and adaptation to cellular stresses in eukaryotic cells. Oxidative stress refers to elevated intracellular levels of reactive oxygen species (ROS) that cause damage to lipids, proteins, and DNA. Oxidative stress has been linked to a myriad of pathologies. Autophagy can be involved in various biological processes such as programmed cell death, stress responses, removal of damaged organelles, and growth. The role of autophagy has been identified as a critical mediator in the pathological response to redox signaling. Autophagy is considered a main sensor of redox signaling. Reactive oxygen species (ROS) are highly reactive molecules produced as byproducts of cellular metabolism, mainly by mitochondria. Mitochondrial reactive oxygen species (mROS) can be beneficial or harmful to cells depending on their concentration and location. Mitochondrial reactive oxygen species (mROS) at low physiological concentrations act as redox messengers in intracellular signaling, while overproduction of mROS causes oxidative damage to cellular components and ultimately leads to cell death. Hence, the balance of stress adaptation associated with autophagy and cell death is important for understanding pathogenesis related to redox signaling. Autophagy is an integral biological process critical for cellular and organismal homeostasis. It allows spatial reorganization and energy supply to cells through the regular destruction machinery of unnecessary or inefficient components. In this review, we focus on the basic mechanisms and functions of autophagy in response to oxidative stress and redox signaling in pathology.

کلیدواژه ها:

Autophagy ، Homeostasis ، mROS ، oxidative stress