This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Griendling, K. K. Search for Related Content PubMed PubMed Citation Articles by Griendling, K. K. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB NITRIC OXIDE Related Collections Redox Mechanisms in Blood Vessels Related Article

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:272.)
© 2005 American Heart Association, Inc.

Brief Reviews

ATVB In Focus

Redox Mechanisms in Blood Vessels

Kathy K. Griendling

From the Division of Cardiology, Emory University, Atlanta, GA 30322

Correspondence to Kathy K. Griendling, Emory University, Division of Cardiology, 319 WMB 1639 Pierce Dr., Atlanta, GA 30322. E-mail kgriend@emory.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Much interest has been generated recently concerning the role of reactive oxygen species (ROS) in vascular health and disease. The original "oxidative modification hypothesis of atherosclerosis" put forth in the early 1980’s by Steinberg and colleagues suggested that oxidative modification of LDL enhanced its atherogenic properties. An explosion of articles in this area substantiated the role of oxidized LDL in atherosclerosis (reviewed by Chisolm and Steinberg¹), but recent work has expanded this hypothesis to include a role for free radicals in hypertension,² the processes leading to restenosis after balloon angioplasty,³ vascular inflammation,⁴ diabetic vascular disease,⁵ and angiogenesis.⁶ Perhaps more importantly, ROS are essential to the normal functioning of the vessel wall, including endothelium-dependent relaxation, contraction, and the smooth muscle cell and endothelial cell growth and survival involved in repair and remodeling of the vessel wall. These diverse and critical roles of ROS in vascular physiology and pathophysiology make understanding the sources of ROS generation of vital importance in the design of therapeutic interventions.

See page 274

Traditionally, macrophages have been assumed to be the source of most of the ROS in the vessel wall. There is no doubt that these cells are powerful ROS generators and that they play an important role in vessel pathology. However, it has become clear that virtually all cells in the vessel wall produce ROS, in varying amounts and in response to diverse stimuli. Endothelial cells, smooth muscle cells, and adventitial cells all produce ROS, which can then act in an autocrine or paracrine . . . [Full Text of this Article]

Related Article:

Redox Mechanisms in Blood Vessels

Cornelius F.H. Mueller, Karine Laude, J. Scott McNally, and David G. Harrison
Arterioscler Thromb Vasc Biol 2005 25: 274-278. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				E. Nozik-Grayck, H. B. Suliman, S. Majka, J. Albietz, Z. Van Rheen, K. Roush, and K. R. Stenmark Lung EC-SOD overexpression attenuates hypoxic induction of Egr-1 and chronic hypoxic pulmonary vascular remodeling Am J Physiol Lung Cell Mol Physiol, September 1, 2008; 295(3): L422 - L430. [Abstract] [Full Text] [PDF]

				J. I. Mendez, W. J. Nicholson, and W. R. Taylor SOD Isoforms and Signaling in Blood Vessels: Evidence for the Importance of ROS Compartmentalization Arterioscler Thromb Vasc Biol, May 1, 2005; 25(5): 887 - 888. [Full Text] [PDF]