Protective Features of Autophagy in Pulmonary Infection and Inflammatory Diseases

Wang, Kui; Chen, Yi; Zhang, Pengju; Lin, Ping; Xie, Na; Wu, Min

doi:10.3390/cells8020123

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Protective Features of Autophagy in Pulmonary Infection and Inflammatory Diseases

by

Kui Wang

^1,2,†,

Yi Chen

^3,†,

Pengju Zhang

¹,

Ping Lin

²,

Na Xie

^1,4,*

and

Min Wu

^2,*

¹

West China School of Basic Medical Sciences & Forensic Medicine, and State Key Laboratory of Biotherapy, Sichuan University, and Collaborative Innovation Center for Biotherapy, Chengdu 610041, China

²

Department of Biomedical Sciences, University of North Dakota, Grand Forks, ND 58203, USA

³

Department of Gastrointestinal Surgery, State Key Laboratory of Biotherapy, Sichuan University, Chengdu 610041, China

⁴

Section of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089-0641, USA

^*

Authors to whom correspondence should be addressed.

^†

These authors contributed equally to this work.

Cells 2019, 8(2), 123; https://doi.org/10.3390/cells8020123

Submission received: 31 December 2018 / Revised: 29 January 2019 / Accepted: 31 January 2019 / Published: 3 February 2019

(This article belongs to the Special Issue Autophagy in Tissue Injury and Homeostasis)

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Abstract

Autophagy is a highly conserved catabolic process involving autolysosomal degradation of cellular components, including protein aggregates, damaged organelles (such as mitochondria, endoplasmic reticulum, and others), as well as various pathogens. Thus, the autophagy pathway represents a major adaptive response for the maintenance of cellular and tissue homeostasis in response to numerous cellular stressors. A growing body of evidence suggests that autophagy is closely associated with diverse human diseases. Specifically, acute lung injury (ALI) and inflammatory responses caused by bacterial infection or xenobiotic inhalation (e.g., chlorine and cigarette smoke) have been reported to involve a spectrum of alterations in autophagy phenotypes. The role of autophagy in pulmonary infection and inflammatory diseases could be protective or harmful dependent on the conditions. In this review, we describe recent advances regarding the protective features of autophagy in pulmonary diseases, with a focus on ALI, idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD), tuberculosis, pulmonary arterial hypertension (PAH) and cystic fibrosis.

Keywords: Autophagy; inflammation; acute lung injury; idiopathic pulmonary fibrosis; COPD; tuberculosis; PAH; cystic fibrosis

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MDPI and ACS Style

Wang, K.; Chen, Y.; Zhang, P.; Lin, P.; Xie, N.; Wu, M. Protective Features of Autophagy in Pulmonary Infection and Inflammatory Diseases. Cells 2019, 8, 123. https://doi.org/10.3390/cells8020123

AMA Style

Wang K, Chen Y, Zhang P, Lin P, Xie N, Wu M. Protective Features of Autophagy in Pulmonary Infection and Inflammatory Diseases. Cells. 2019; 8(2):123. https://doi.org/10.3390/cells8020123

Chicago/Turabian Style

Wang, Kui, Yi Chen, Pengju Zhang, Ping Lin, Na Xie, and Min Wu. 2019. "Protective Features of Autophagy in Pulmonary Infection and Inflammatory Diseases" Cells 8, no. 2: 123. https://doi.org/10.3390/cells8020123

APA Style

Wang, K., Chen, Y., Zhang, P., Lin, P., Xie, N., & Wu, M. (2019). Protective Features of Autophagy in Pulmonary Infection and Inflammatory Diseases. Cells, 8(2), 123. https://doi.org/10.3390/cells8020123

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

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Protective Features of Autophagy in Pulmonary Infection and Inflammatory Diseases

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