A role for acute-phase serum amyloid A and high-density lipoprotein in oxidative stress, endothelial dysfunction and atherosclerosis

Authors: Hua, Susan1; Song, Changjie1; Geczy, Carolyn2; Freedman, S. Ben1; Witting, Paul3

Source: Redox Report, Volume 14, Number 5, October 2009 , pp. 187-196(10)

Publisher: Maney Publishing

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Abstract:

The acute-phase protein serum amyloid A (SAA) is a clinically useful marker of inflammation and associates strongly with increased risk of cardiovascular events. Chronically elevated SAA concentrations may contribute to physiological processes that lead to atherosclerosis, including endothelial dysfunction, an early and predictive event in the development of cardiovascular disease. Accumulating data suggest that SAA can be a direct mediator in the development and progression of atherogenesis and atherothrombosis. SAA may affect key events underlying acute coronary syndromes, including cholesterol transport, contribute to endothelial dysfunction, promote thrombosis, and enhance leukocyte trafficking and activation. This review summarizes the evidence supporting a role for SAA as a potential regulator of inflammation and endothelial dysfunction, which underlie the adverse outcomes that complicate coronary artery disease. The findings suggest that novel therapeutic strategies to reduce SAA levels and/or oppose the actions of SAA may have beneficial effects in patients with coronary artery disease.

Keywords: ENDOTHELIAL DYSFUNCTION; OXIDATIVE STRESS; HIGH-DENSITY LIPOPROTEIN; ATHEROSCLEROSIS; SERUM AMYLOID A; CORONARY ARTERY DISEASE

Document Type: Review Article

DOI: http://dx.doi.org/10.1179/135100009X12525712409490

Affiliations: 1: Vascular Biology Group, ANZAC Research Institute, Concord Repatriation General Hospital, Sydney Medical School, University of Sydney, Concord, New South Wales, Australia 2: Cytokine Biology Group, School of Medical Sciences, University of New South Wales, New South Wales, Australia 3: Vascular Biology Group, ANZAC Research Institute, Concord Repatriation General Hospital, Sydney Medical School, University of Sydney, Concord, New South Wales, Australia; Discipline of Pathology, Bosch Institute, Sydney Medical School, The University of Sydney, New South Wales, Australia

Publication date: 2009-10-01

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