Redox mechanisms in age-related lung fibrosis

Redox signaling and oxidative stress are associated with tissue fibrosis and aging. Aging is recognized as a major risk factor for fibrotic diseases involving multiple organ systems, including that of the lung. A number of oxidant generating enzymes are upregulated while antioxidant defenses are def...

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Main Authors: Ashish Kurundkar, Victor J. Thannickal
Format: Article
Language:English
Published: Elsevier 2016-10-01
Series:Redox Biology
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2213231716300519
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spelling doaj-fcc66c17e2db4b51a305abddaaead2092020-11-24T22:09:53ZengElsevierRedox Biology2213-23172016-10-019C677610.1016/j.redox.2016.06.005Redox mechanisms in age-related lung fibrosisAshish KurundkarVictor J. ThannickalRedox signaling and oxidative stress are associated with tissue fibrosis and aging. Aging is recognized as a major risk factor for fibrotic diseases involving multiple organ systems, including that of the lung. A number of oxidant generating enzymes are upregulated while antioxidant defenses are deficient with aging and cellular senescence, leading to redox imbalance and oxidative stress. However, the precise mechanisms by which redox signaling and oxidative stress contribute to the pathogenesis of lung fibrosis are not well understood. Tissue repair is a highly regulated process that involves the interactions of several cell types, including epithelial cells, fibroblasts and inflammatory cells. Fibrosis may develop when these interactions are dysregulated with the acquisition of pro-fibrotic cellular phenotypes. In this review, we explore the roles of redox mechanisms that promote and perpetuate fibrosis in the context of cellular senescence and aging.http://www.sciencedirect.com/science/article/pii/S2213231716300519Oxidative stressSenescenceMyofibroblastsInflammationEpithelial cells
collection DOAJ
language English
format Article
sources DOAJ
author Ashish Kurundkar
Victor J. Thannickal
spellingShingle Ashish Kurundkar
Victor J. Thannickal
Redox mechanisms in age-related lung fibrosis
Redox Biology
Oxidative stress
Senescence
Myofibroblasts
Inflammation
Epithelial cells
author_facet Ashish Kurundkar
Victor J. Thannickal
author_sort Ashish Kurundkar
title Redox mechanisms in age-related lung fibrosis
title_short Redox mechanisms in age-related lung fibrosis
title_full Redox mechanisms in age-related lung fibrosis
title_fullStr Redox mechanisms in age-related lung fibrosis
title_full_unstemmed Redox mechanisms in age-related lung fibrosis
title_sort redox mechanisms in age-related lung fibrosis
publisher Elsevier
series Redox Biology
issn 2213-2317
publishDate 2016-10-01
description Redox signaling and oxidative stress are associated with tissue fibrosis and aging. Aging is recognized as a major risk factor for fibrotic diseases involving multiple organ systems, including that of the lung. A number of oxidant generating enzymes are upregulated while antioxidant defenses are deficient with aging and cellular senescence, leading to redox imbalance and oxidative stress. However, the precise mechanisms by which redox signaling and oxidative stress contribute to the pathogenesis of lung fibrosis are not well understood. Tissue repair is a highly regulated process that involves the interactions of several cell types, including epithelial cells, fibroblasts and inflammatory cells. Fibrosis may develop when these interactions are dysregulated with the acquisition of pro-fibrotic cellular phenotypes. In this review, we explore the roles of redox mechanisms that promote and perpetuate fibrosis in the context of cellular senescence and aging.
topic Oxidative stress
Senescence
Myofibroblasts
Inflammation
Epithelial cells
url http://www.sciencedirect.com/science/article/pii/S2213231716300519
work_keys_str_mv AT ashishkurundkar redoxmechanismsinagerelatedlungfibrosis
AT victorjthannickal redoxmechanismsinagerelatedlungfibrosis
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