Autophagy in pulmonary fibrosis: friend or foe?
Autophagy in pulmonary fibrosis: friend or foe?
Autophagy is an evolutionarily conserved process where long-lived and damaged organelles are degraded. Autophagy has been widely associated with several ageing-process as well in diseases such as neurodegeneration, cancer and fibrosis, and is now being utilised as a target in these diseases. Idiopathic pulmonary fibrosis (IPF) is a progressive, interstitial lung disease with limited treatment options available. It is characterised by abnormal extracellular matrix (ECM) deposition by activated myofibroblasts. It is understood that repetitive micro-injuries to aged-alveolar epithelium combined with genetic factors drive the disease. Several groups have demonstrated that autophagy is altered in IPF although whether autophagy has a protective effect or not is yet to be determined. Autophagy has also been shown to influence many other processes including epithelial mesenchymal transition (EMT) and endothelial mesenchymal transition (EndMT) which are known to be key in the pathogenesis of IPF. In this review, we summarise the findings of evidence of altered autophagy in IPF lungs, as well as examine its roles within lung fibrosis. Given these findings, together with the growing use of autophagy manipulation in a clinical setting, this is an exciting area for further research in the study of lung fibrosis.
1594-1607
Hill, Charlotte
6d1cfed3-11b1-48af-b171-b8726ab673eb
Wang, Yihua
f5044a95-60a7-42d2-87d6-5f1f789e3a7e
1 November 2022
Hill, Charlotte
6d1cfed3-11b1-48af-b171-b8726ab673eb
Wang, Yihua
f5044a95-60a7-42d2-87d6-5f1f789e3a7e
Abstract
Autophagy is an evolutionarily conserved process where long-lived and damaged organelles are degraded. Autophagy has been widely associated with several ageing-process as well in diseases such as neurodegeneration, cancer and fibrosis, and is now being utilised as a target in these diseases. Idiopathic pulmonary fibrosis (IPF) is a progressive, interstitial lung disease with limited treatment options available. It is characterised by abnormal extracellular matrix (ECM) deposition by activated myofibroblasts. It is understood that repetitive micro-injuries to aged-alveolar epithelium combined with genetic factors drive the disease. Several groups have demonstrated that autophagy is altered in IPF although whether autophagy has a protective effect or not is yet to be determined. Autophagy has also been shown to influence many other processes including epithelial mesenchymal transition (EMT) and endothelial mesenchymal transition (EndMT) which are known to be key in the pathogenesis of IPF. In this review, we summarise the findings of evidence of altered autophagy in IPF lungs, as well as examine its roles within lung fibrosis. Given these findings, together with the growing use of autophagy manipulation in a clinical setting, this is an exciting area for further research in the study of lung fibrosis.
Text
JJ-LQY-ZGW-21-222 Autophagy-fibrosis-review-rev-v3-clean_EA_CH_YW
- Accepted Manuscript
More information
Accepted/In Press date: 24 September 2021
e-pub ahead of print date: 23 October 2021
Published date: 1 November 2022
Additional Information:
Funding Information:
This work was supported by the Medical Research Council (No. MR/S025480/1), the Academy of Medical Sciences/the Wellcome Trust Springboard Award (No. SBF002\1038), Wessex Medical Trust and AAIR Charity. CH was supported by Gerald Kerkut Charitable Trust and University of Southampton Central VC Scholarship Scheme.
Funding Information:
This work was supported by the Medical Research Council (No. MR/S025480/1 ), the Academy of Medical Sciences /the Wellcome Trust Springboard Award (No. SBF002\1038 ), Wessex Medical Trust and AAIR Charity . CH was supported by Gerald Kerkut Charitable Trust and University of Southampton Central VC Scholarship Scheme .
Publisher Copyright:
© 2021 Chongqing Medical University
Identifiers
Local EPrints ID: 452100
URI: http://eprints.soton.ac.uk/id/eprint/452100
ISSN: 2352-3042
PURE UUID: 01315cd9-e5d0-4f58-949b-be1dc106ad78
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Date deposited: 11 Nov 2021 17:37
Last modified: 17 Mar 2024 03:39
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Author:
Charlotte Hill
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