<i>S</i>-Glutathionylation-Controlled Apoptosis of Lung Epithelial Cells; Potential Implications for Lung Fibrosis

Glutathione (GSH), a major antioxidant in mammalian cells, regulates several vital cellular processes, such as nutrient metabolism, protein synthesis, and immune responses. In addition to its role in antioxidant defense, GSH controls biological processes through its conjugation to reactive protein c...

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Main Authors: Elizabeth Corteselli, Reem Aboushousha, Yvonne Janssen-Heininger
Format: Article
Language:English
Published: MDPI AG 2022-09-01
Series:Antioxidants
Subjects:
Online Access:https://www.mdpi.com/2076-3921/11/9/1789
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author Elizabeth Corteselli
Reem Aboushousha
Yvonne Janssen-Heininger
author_facet Elizabeth Corteselli
Reem Aboushousha
Yvonne Janssen-Heininger
author_sort Elizabeth Corteselli
collection DOAJ
description Glutathione (GSH), a major antioxidant in mammalian cells, regulates several vital cellular processes, such as nutrient metabolism, protein synthesis, and immune responses. In addition to its role in antioxidant defense, GSH controls biological processes through its conjugation to reactive protein cysteines in a post-translational modification known as protein <i>S</i>-glutathionylation (PSSG). PSSG has recently been implicated in the pathogenesis of multiple diseases including idiopathic pulmonary fibrosis (IPF). Hallmarks of IPF include repeated injury to the alveolar epithelium with aberrant tissue repair, epithelial cell apoptosis and fibroblast resistance to apoptosis, and the accumulation of extracellular matrix and distortion of normal lung architecture. Several studies have linked oxidative stress and PSSG to the development and progression of IPF. Additionally, it has been suggested that the loss of epithelial cell homeostasis and increased apoptosis, accompanied by the release of various metabolites, creates a vicious cycle that aggravates disease progression. In this short review, we highlight some recent studies that link PSSG to epithelial cell apoptosis and highlight the potential implication of metabolites secreted by apoptotic cells.
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spelling doaj.art-78a3799e2c224ceeb5c9aa7cfd0cd2472023-11-23T14:48:55ZengMDPI AGAntioxidants2076-39212022-09-01119178910.3390/antiox11091789<i>S</i>-Glutathionylation-Controlled Apoptosis of Lung Epithelial Cells; Potential Implications for Lung FibrosisElizabeth Corteselli0Reem Aboushousha1Yvonne Janssen-Heininger2Department of Pathology and Laboratory of Medicine, University of Vermont Larner College of Medicine, Burlington, VT 05405, USADepartment of Pathology and Laboratory of Medicine, University of Vermont Larner College of Medicine, Burlington, VT 05405, USADepartment of Pathology and Laboratory of Medicine, University of Vermont Larner College of Medicine, Burlington, VT 05405, USAGlutathione (GSH), a major antioxidant in mammalian cells, regulates several vital cellular processes, such as nutrient metabolism, protein synthesis, and immune responses. In addition to its role in antioxidant defense, GSH controls biological processes through its conjugation to reactive protein cysteines in a post-translational modification known as protein <i>S</i>-glutathionylation (PSSG). PSSG has recently been implicated in the pathogenesis of multiple diseases including idiopathic pulmonary fibrosis (IPF). Hallmarks of IPF include repeated injury to the alveolar epithelium with aberrant tissue repair, epithelial cell apoptosis and fibroblast resistance to apoptosis, and the accumulation of extracellular matrix and distortion of normal lung architecture. Several studies have linked oxidative stress and PSSG to the development and progression of IPF. Additionally, it has been suggested that the loss of epithelial cell homeostasis and increased apoptosis, accompanied by the release of various metabolites, creates a vicious cycle that aggravates disease progression. In this short review, we highlight some recent studies that link PSSG to epithelial cell apoptosis and highlight the potential implication of metabolites secreted by apoptotic cells.https://www.mdpi.com/2076-3921/11/9/1789glutaredoxinglutathioneapoptosisidiopathic pulmonary fibrosisepithelial cells
spellingShingle Elizabeth Corteselli
Reem Aboushousha
Yvonne Janssen-Heininger
<i>S</i>-Glutathionylation-Controlled Apoptosis of Lung Epithelial Cells; Potential Implications for Lung Fibrosis
Antioxidants
glutaredoxin
glutathione
apoptosis
idiopathic pulmonary fibrosis
epithelial cells
title <i>S</i>-Glutathionylation-Controlled Apoptosis of Lung Epithelial Cells; Potential Implications for Lung Fibrosis
title_full <i>S</i>-Glutathionylation-Controlled Apoptosis of Lung Epithelial Cells; Potential Implications for Lung Fibrosis
title_fullStr <i>S</i>-Glutathionylation-Controlled Apoptosis of Lung Epithelial Cells; Potential Implications for Lung Fibrosis
title_full_unstemmed <i>S</i>-Glutathionylation-Controlled Apoptosis of Lung Epithelial Cells; Potential Implications for Lung Fibrosis
title_short <i>S</i>-Glutathionylation-Controlled Apoptosis of Lung Epithelial Cells; Potential Implications for Lung Fibrosis
title_sort i s i glutathionylation controlled apoptosis of lung epithelial cells potential implications for lung fibrosis
topic glutaredoxin
glutathione
apoptosis
idiopathic pulmonary fibrosis
epithelial cells
url https://www.mdpi.com/2076-3921/11/9/1789
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