Next Article in Journal
How Can Plant DNA Viruses Evade siRNA-Directed DNA Methylation and Silencing?
Next Article in Special Issue
Mild Oxidative Damage in the Diabetic Rat Heart Is Attenuated by Glyoxalase-1 Overexpression
Previous Article in Journal
Anti-Inflammatory Activity of N-(3-Florophenyl)ethylcaffeamide in Mice
Previous Article in Special Issue
Chlamydia pneumoniae Infection in Atherosclerotic Lesion Development through Oxidative Stress: A Brief Overview
Article Menu

Export Article

Open AccessReview
Int. J. Mol. Sci. 2013, 14(8), 15212-15232; doi:10.3390/ijms140815212

S-Glutathionylation in Monocyte and Macrophage (Dys)Function

1
Department of Biochemistry, University of Texas Health Science Center San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA
2
Department of Clinical Laboratory Sciences, University of Texas Health Science Center San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA
*
Author to whom correspondence should be addressed.
Received: 3 June 2013 / Revised: 15 June 2013 / Accepted: 18 June 2013 / Published: 24 July 2013
(This article belongs to the Special Issue Oxidative Stress in Cardiovascular Disease)
View Full-Text   |   Download PDF [240 KB, uploaded 19 June 2014]   |  

Abstract

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. View Full-Text
Keywords: S-glutathionylation; monocyte; macrophage; thiol oxidative stress; vascular diseases S-glutathionylation; monocyte; macrophage; thiol oxidative stress; vascular diseases
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Ullevig, S.; Kim, H.S.; Asmis, R. S-Glutathionylation in Monocyte and Macrophage (Dys)Function. Int. J. Mol. Sci. 2013, 14, 15212-15232.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top