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Autophagy, selective autophagy, and necroptosis in COPD

Authors Mizumura K, Maruoka S, Shimizu T, Gon Y

Received 30 May 2018

Accepted for publication 1 August 2018

Published 9 October 2018 Volume 2018:13 Pages 3165—3172


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Richard Russell

Kenji Mizumura, Shuichiro Maruoka, Tetsuo Shimizu, Yasuhiro Gon

Division of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan

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

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