© 2004 by BMJ Publishing Group & British Cardiac Society
MINI-SYMPOSIUM
SOXF: redox mediators of vascular smooth muscle cell growth
Center for Cardiovascular Research, University of Rochester, New York, USA
Correspondence to:
Correspondence to:
Bradford C Berk MD PhD
University of Rochester, Department of Medicine, Box MED, Rochester, NY 14642, USA; bradford_berk{at}urmc.rochester.edu
Keywords: oxidative stress; heat shock proteins; cyclophilin A; vascular smooth muscle; signal transduction; atherosclerosis
Abbreviations: Ang II, angiotensin II; CyPA, cyclophilin A; ERK, extracellular regulated signal kinase; HSP90, heat shock protein 90; PDGF, platelet derived growth factor; PPIase, peptidyl-prolyl cis-trans isomerase; ROS, reactive oxygen species; SOXF, secreted oxidative stress induced factors; VSMC, vascular smooth muscle cells
| The first 150 words of the full text of this article appear below. |
Oxidative stress and the production of intracellular reactive oxygen species (ROS), such as superoxide (O2.), hydrogen peroxide (H2O2), and hydroxyl radical (OH.), have been implicated in the pathogenesis of cardiovascular disease, in part by promoting vascular smooth muscle proliferation.14 Within the vessel wall, ROS are generated by several mechanisms, including vascular NAD(P)H oxidases.5,6 ROS formation can be stimulated by mechanical stress, environmental factors, platelet derived growth factor (PDGF), angiotensin II (Ang II), and low density lipoproteins.79 Because many risk factors for coronary artery disease such as hyperlipidaemia, hypertension, diabetes, and smoking increase production of ROS, it has been suggested that changes in vessel redox state are a common pathway involved in the pathogenesis of atherosclerosis and vascular injury.1,6,10
Several key findings support the concept that ROS contribute to vascular diseases through effects on vascular smooth muscle cells (VSMC). Initial studies in our laboratory demonstrated that ROS
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