<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...
Main Authors: | , , |
---|---|
Format: | Article |
Language: | English |
Published: |
MDPI AG
2022-09-01
|
Series: | Antioxidants |
Subjects: | |
Online Access: | https://www.mdpi.com/2076-3921/11/9/1789 |
_version_ | 1797491690175463424 |
---|---|
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. |
first_indexed | 2024-03-10T00:52:57Z |
format | Article |
id | doaj.art-78a3799e2c224ceeb5c9aa7cfd0cd247 |
institution | Directory Open Access Journal |
issn | 2076-3921 |
language | English |
last_indexed | 2024-03-10T00:52:57Z |
publishDate | 2022-09-01 |
publisher | MDPI AG |
record_format | Article |
series | Antioxidants |
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 |
work_keys_str_mv | AT elizabethcorteselli isiglutathionylationcontrolledapoptosisoflungepithelialcellspotentialimplicationsforlungfibrosis AT reemaboushousha isiglutathionylationcontrolledapoptosisoflungepithelialcellspotentialimplicationsforlungfibrosis AT yvonnejanssenheininger isiglutathionylationcontrolledapoptosisoflungepithelialcellspotentialimplicationsforlungfibrosis |