Autophagy, selective autophagy, and necroptosis in COPD

Abstract

COPD is characterized by persistent respiratory symptoms and airflow limitation, caused by a mixture of small airway disease and pulmonary emphysema. Programmed cell death has drawn the attention of COPD researchers because emphysema is thought to result from epithelial cell death caused by smoking. Although apoptosis has long been thought to be the sole form of programmed cell death, recent studies have reported the existence of a genetically programmed and regulated form of necrosis called necroptosis. Autophagy was also previously considered a form of programmed cell death, but this has been reconsidered. However, recent studies have revealed that autophagy can regulate programmed cell death, including apoptosis and necroptosis. It is also becoming clear that autophagy can selectively degrade specific proteins, organelles, and invading bacteria by a process termed “selective autophagy” and that this process is related to the pathogenesis of human diseases. In this review, we outline the most recent studies implicating autophagy, selective autophagy, and necroptosis in COPD. Strategies targeting these pathways may yield novel therapies for COPD.

Keywords:

• ciliophagy
• mitophagy
• programmed cell death
• pulmonary emphysema

Acknowledgments

The authors are grateful to Augustine MK Choi for collaboration and suggesting the topic treated in this article.

Author contributions

KM, SM, TS, and YG designed the strategy and goal of this review. KM drafted the article. All authors read and approved the final manuscript. All authors contributed to data analysis, drafting and revising the article, gave final approval of the version to be published, and agree to be accountable for all aspects of the work.

Disclosure

The authors report no conflicts of interest in this work.