The interplay between oxidative stress and autophagy in chronic obstructive pulmonary disease

Autophagy is a highly conserved process that is indispensable for cell survival, embryonic development, and tissue homeostasis. Activation of autophagy protects cells against oxidative stress and is a major adaptive response to injury. When autophagy is dysregulated by factors such as smoking, environmental insults and aging, it can lead to enhanced formation of aggressors and production of reactive oxygen species (ROS), resulting in oxidative stress and oxidative damage to cells. ROS activates autophagy, which in turn promotes cell adaptation and reduces oxidative damage by degrading and circulating damaged macromolecules and dysfunctional cell organelles. The cellular response triggered by oxidative stress includes changes in signaling pathways that ultimately regulate autophagy. Chronic obstructive pulmonary disease (COPD) is the most common lung disease among the elderly worldwide, with a high mortality rate. As an induced response to oxidative stress, autophagy plays an important role in the pathogenesis of COPD. This review discusses the regulation of oxidative stress and autophagy in COPD, and aims to provide new avenues for future research on target-specific treatments for COPD.

Automated summary

Autophagy is a crucial process for cell survival, development, and tissue balance. It protects cells against oxidative stress and injury. Dysregulated autophagy caused by factors like smoking and aging can lead to increased production of reactive oxygen species (ROS) and oxidative damage. ROS activates autophagy, which helps cells adapt and reduce damage by eliminating damaged molecules and organelles. Understanding the regulation of oxidative stress and autophagy is important in chronic obstructive pulmonary disease (COPD) research.