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S-Glutathionylation in Monocyte and Macrophage (Dys)Function
Atherosclerosis is a chronic inflammatory disease involving the accumulation of monocytes and macrophages in the vascular wall. Monocytes and macrophages play a central role in the initiation and progression of atherosclerotic lesion development. Oxidative stress, which occurs when reactive oxygen s...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3759857/ https://www.ncbi.nlm.nih.gov/pubmed/23887649 http://dx.doi.org/10.3390/ijms140815212 |
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author | Ullevig, Sarah Kim, Hong Seok Asmis, Reto |
author_facet | Ullevig, Sarah Kim, Hong Seok Asmis, Reto |
author_sort | Ullevig, Sarah |
collection | PubMed |
description | Atherosclerosis is a chronic inflammatory disease involving the accumulation of monocytes and macrophages in the vascular wall. Monocytes and macrophages play a central role in the initiation and progression of atherosclerotic lesion development. Oxidative stress, which occurs when reactive oxygen species (ROS) overwhelm cellular antioxidant systems, contributes to the pathophysiology of many chronic inflammatory diseases, including atherosclerosis. Major targets of ROS are reactive thiols on cysteine residues in proteins, which when oxidized can alter cellular processes, including signaling pathways, metabolic pathways, transcription, and translation. Protein-S-glutathionylation is the process of mixed disulfide formation between glutathione (GSH) and protein thiols. Until recently, protein-S-glutathionylation was associated with increased cellular oxidative stress, but S-glutathionylation of key protein targets has now emerged as a physiologically important redox signaling mechanism, which when dysregulated contributes to a variety of disease processes. In this review, we will explore the role of thiol oxidative stress and protein-S-glutathionylation in monocyte and macrophage dysfunction as a mechanistic link between oxidative stress associated with metabolic disorders and chronic inflammatory diseases, including atherosclerosis. |
format | Online Article Text |
id | pubmed-3759857 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-37598572013-09-03 S-Glutathionylation in Monocyte and Macrophage (Dys)Function Ullevig, Sarah Kim, Hong Seok Asmis, Reto Int J Mol Sci Review Atherosclerosis is a chronic inflammatory disease involving the accumulation of monocytes and macrophages in the vascular wall. Monocytes and macrophages play a central role in the initiation and progression of atherosclerotic lesion development. Oxidative stress, which occurs when reactive oxygen species (ROS) overwhelm cellular antioxidant systems, contributes to the pathophysiology of many chronic inflammatory diseases, including atherosclerosis. Major targets of ROS are reactive thiols on cysteine residues in proteins, which when oxidized can alter cellular processes, including signaling pathways, metabolic pathways, transcription, and translation. Protein-S-glutathionylation is the process of mixed disulfide formation between glutathione (GSH) and protein thiols. Until recently, protein-S-glutathionylation was associated with increased cellular oxidative stress, but S-glutathionylation of key protein targets has now emerged as a physiologically important redox signaling mechanism, which when dysregulated contributes to a variety of disease processes. In this review, we will explore the role of thiol oxidative stress and protein-S-glutathionylation in monocyte and macrophage dysfunction as a mechanistic link between oxidative stress associated with metabolic disorders and chronic inflammatory diseases, including atherosclerosis. MDPI 2013-07-24 /pmc/articles/PMC3759857/ /pubmed/23887649 http://dx.doi.org/10.3390/ijms140815212 Text en © 2013 by the authors; licensee MDPI, Basel, Switzerland http://creativecommons.org/licenses/by/3.0 This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Review Ullevig, Sarah Kim, Hong Seok Asmis, Reto S-Glutathionylation in Monocyte and Macrophage (Dys)Function |
title | S-Glutathionylation in Monocyte and Macrophage (Dys)Function |
title_full | S-Glutathionylation in Monocyte and Macrophage (Dys)Function |
title_fullStr | S-Glutathionylation in Monocyte and Macrophage (Dys)Function |
title_full_unstemmed | S-Glutathionylation in Monocyte and Macrophage (Dys)Function |
title_short | S-Glutathionylation in Monocyte and Macrophage (Dys)Function |
title_sort | s-glutathionylation in monocyte and macrophage (dys)function |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3759857/ https://www.ncbi.nlm.nih.gov/pubmed/23887649 http://dx.doi.org/10.3390/ijms140815212 |
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