Basic mechanisms of oxidative stress and reactive oxygen species in cardiovascular injury

• Type of Material: Article
• Authors: Christopher A Papaharalambus, Emory University; Kathy Griendling, Emory University
• Language: English
• Date: 2007-02
• Publisher: Elsevier: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2007 Elsevier Inc. All rights reserved.
• License: Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported
• Final Published Version (URL): http://dx.doi.org/10.1016/j.tcm.2006.11.005
• Title of Journal or Parent Work: Trends in Cardiovascular Medicine
• ISSN: 1050-1738
• Volume: 17
• Issue: 2
• Start Page: 48
• End Page: 54
• Grant/Funding Information: This work was supported by NIH grants HL058000, HL038206, and HL058863.
• Research Categories: Biology, Physiology; Health Sciences, Pathology; Health Sciences, Rehabilitation and Therapy

Abstract

The development of vascular disease has its origins in an initial insult to the vessel wall by biological or mechanical factors. The disruption of homeostatic mechanisms leads to alteration of the original architecture of the vessel and its biological responsiveness, contributing to acute or chronic diseases such as stroke, hypertension and atherosclerosis. Endothelial dysfunction, macrophage infiltration of the vessel wall, and proliferation and migration of smooth muscle cells all involve different types of reactive oxygen species, produced by various vessel wall components. Although basic science and animal research have clearly established the role of reactive oxygen species in the progression of vascular disease, the failure of clinical trials with antioxidant compounds has underscored the need for better antioxidant therapies and a more thorough understanding of the role of reactive oxygen species in cardiovascular physiology and pathology.