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Recent evidence from omic analysis for redox signalling and mitochondrial oxidative stress in COPD

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Mumby Adcock COPD Omics ROS Mitochondrial J Inflammation revised unmarked2.docxAccepted version87.34 kBMicrosoft WordView/Open
Title: Recent evidence from omic analysis for redox signalling and mitochondrial oxidative stress in COPD
Authors: Adcock, I
Mumby, S
Item Type: Journal Article
Abstract: COPD is driven by exogenous and endogenous oxidative stress derived from inhaled cigarette smoke, air pollution and reactive oxygen species from dysregulated mitochondria in activated inflammatory cells within the airway and lung. This is compounded by the loss in antioxidant defences including FOXO and NRF2 and other antioxidant transcription factors together with various key enzymes that attenuate oxidant effects. Oxidative stress enhances inflammation; airway remodelling including fibrosis and emphysema; post-translational protein modifications leading to autoantibody generation; DNA damage and cellular senescence. Recent studies using various omics technologies in the airways, lungs and blood of COPD patients has emphasised the importance of oxidative stress, particularly that derived from dysfunctional mitochondria in COPD and its role in immunity, inflammation, mucosal barrier function and infection. Therapeutic interventions targeting oxidative stress should overcome the deleterious pathologic effects of COPD if targeted to the lung. We require novel, more efficacious antioxidant COPD treatments among which mitochondria-targeted antioxidants and Nrf2 activators are promising.
Date of Acceptance: 27-Jun-2022
URI: http://hdl.handle.net/10044/1/97973
ISSN: 1476-9255
Publisher: BioMed Central
Journal / Book Title: Journal of Inflammation
Volume: 19
Copyright Statement: © The Author(s) 2022. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativeco mmons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
Sponsor/Funder: Wellcome Trust
Engineering & Physical Science Research Council (EPSRC)
Medical Research Council (MRC)
Funder's Grant Number: 208340/Z/17/Z
EP/T003189/1
MR/T010371/1
Keywords: Science & Technology
Life Sciences & Biomedicine
Immunology
COPD
Transcriptomics
Mitochondria
Oxidative stress
OBSTRUCTIVE PULMONARY-DISEASE
AIRWAY EPITHELIAL-CELLS
CIGARETTE-SMOKE
LUNG
EMPHYSEMA
IRON
EXPRESSION
SIGNATURE
REVEALS
COPD
Mitochondria
Oxidative stress
Transcriptomics
Immunology
1103 Clinical Sciences
1115 Pharmacology and Pharmaceutical Sciences
Publication Status: Published
Appears in Collections:National Heart and Lung Institute
Faculty of Medicine



This item is licensed under a Creative Commons License Creative Commons