The Multifaceted Roles of Autophagy in Infectious, Obstructive, and Malignant Airway Diseases

Our plain-English summary of The Multifaceted Roles of Autophagy in Infectious, Obstructive, and Malignant Airway Diseases, by M. Carinci, L. Palumbo, G. Pellielo, et al (Biomedicines, 2022).

The study

• Authors: M. Carinci, L. Palumbo, G. Pellielo, E.D. Agyapong, G. Morciano, S. Patergnani, C. Giorgi, P. Pinton, A. Rimessi
• Journal: Biomedicines
• Published: 2022;10(8)
• Type of article: Review
• Cited by: 7 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Autophagy is a highly conserved dynamic process by which cells deliver their contents to lysosomes for degradation, thus ensuring cell homeostasis. In response to environmental stress, the induction of autophagy is crucial for cell survival. The dysregulation of this degradative process has been implicated in a wide range of pathologies, including lung diseases, representing a relevant potential target with significant clinical outcomes. During lung disease progression and infections, autophagy may exert both protective and harmful effects on cells. In this review, we will explore the implications of autophagy and its selective forms in several lung infections, such as SARS-CoV-2, Respiratory Syncytial Virus (RSV) and Mycobacterium tuberculosis (Mtb) infections, and different lung diseases such as Cystic Fibrosis (CF), Chronic Obstructive Pulmonary Disease (COPD), and Malignant Mesothelioma (MM).

In plain English

This article was a review, not an original study. The authors, from the University of Ferrara in Italy, described published research on autophagy, the process by which cells break down and recycle their own contents. They covered lung infections (SARS-CoV-2, Respiratory Syncytial Virus and Mycobacterium tuberculosis) and lung diseases (cystic fibrosis, COPD and malignant mesothelioma). In the mesothelioma section, they described mesothelioma as primarily associated with exposure to carcinogenic mineral fibers, particularly asbestos. They summarized earlier work in which human mesothelial cells exposed to carcinogenic fibers showed increased autophagy together with release of a protein called HMGB1. In that work, loss of HMGB1 reduced asbestos-induced autophagy and the cell changes that followed. The authors also reported that increased autophagy had been found in mesothelioma and that it was linked to resistance to several chemotherapy treatments. They noted that there was no direct evidence that BAP1 mutations or SV40 infection affect autophagy in mesothelioma development. The authors concluded that autophagy plays many roles in lung infections and lung disease, both harmful and protective, and that further research is urgently needed.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: narrative review of published research on autophagy in lung infections and lung diseases; no original data
• Who was studied: No study population; the review covered published laboratory, animal and human research on SARS-CoV-2, RSV and Mycobacterium tuberculosis infections, cystic fibrosis, COPD and malignant mesothelioma
• Exposure: For malignant mesothelioma: carcinogenic mineral fibers, particularly asbestos (no fiber types specified in the review text); cigarette smoke was discussed for COPD
• Main results:
  • Reviewed work: human primary mesothelial cells exposed to carcinogenic fibers showed increased autophagy together with release and activation of HMGB1
  • Reviewed work: in experiments using HMGB1 interference or HMGB1-knockout mice, loss of HMGB1 reduced asbestos-induced autophagy and subsequent cell transformation
  • Reviewed work: using the drug desmethylclomipramine as an autophagy inhibitor interfered with asbestos-mediated cell transformation
  • Reviewed work: increased levels of autophagy were found in malignant mesothelioma, and autophagy was linked to resistance to several chemotherapy interventions
  • Reviewed work: a specific ULK1 inhibitor (MRT 68921) reduced excessive autophagy in mesothelioma cells
  • The authors noted that there is no direct evidence that BAP1 mutations or SV40 infection modulate autophagy in the development of mesothelioma
  • For COPD, the review described evidence that autophagy may have both protective and harmful effects
• The authors' conclusion: The authors concluded that autophagy plays many roles, both harmful and protective, in lung infections and lung disease progression, and that further research is urgently needed to develop context-dependent strategies for manipulating it

Topics

Medical terms in this study, explained in our Lexicon: Disease Progression, Fibrosis, COPD, Mesothelioma.

Related studies

• The relative importance of clinical, radiological and pulmonary function variables in evaluating asbestosis and chronic obstructive airway disease in asbestos workers — G.M. Regan, B. Tagg, et al. (1971)
• Obstructive airway disease as a risk factor for asbestos-associated malignancy — P. Harber, A. Oren, et al. (1986)
• Characteristics of airway obstruction severity in relation to air pollutant in asbestos-exposed chronic obstructive pulmonary disease individuals: A cross-sectional study — M. Yu, X. Lu, et al. (2026)
• Infectious disease risk in asbestos abatement workers — J.H. Lange, G. Mastrangelo, et al. (2012)
• Epidemics of non-infectious disease — P.J. Lawther (1979)
• Asbestos induces mesothelial cell transformation via HMGB1-driven autophagy — J. Xue, S. Patergnani, et al. (2020)

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