(Hypertension. 2006;47:803.)
© 2006 American Heart Association, Inc.
Brief Review |
From the Departments of Nephrology and Hypertension (H.C., M.C.V., H.A.K., J.A.J., B.B.) and Vascular Medicine (M.C.V.), University Medical Center Utrecht, Utrecht, the Netherlands.
Correspondence to Branko Braam, Department of Nephrology and Hypertension F03.226, University Medical Center Utrecht, 3508 GA Utrecht, the Netherlands. E-mail bbraam{at}gmail.com
Cardiovascular disease is still hard to predict in an individual. The main focus in cardiovascular research has been on endothelial cells and vascular smooth muscle cells of the vessel wall and their interactions with the blood flow. Alterations in the properties of the blood have received a lot of attention in biochemical terms. Interestingly, alterations in the properties of circulating cells have received less attention. We propose that presence of 1 or more risk factors together with normal physiological stimuli induce redox-dependent changes in leukocyte gene transcription with pathophysiological responses. Thus, risk factors render leukocytes hypersensitive to normal stimuli. Risk factors can be subdivided into physical and chemical factors. Superimposed on physiological regulators of leukocyte function, these risk factors promote a cellular pro-oxidative state. Redox-sensitive transcription factors are activated, leading to responses involving inflammation, adhesion, migration, and additional reactive oxygen species generation. As a consequence, monitoring of individual gene expression signatures of these cells could well increase our understanding of the mechanisms by which leukocytes and, in particular, monocytes function. Furthermore, transcriptomes of these cells could be used to investigate the aggressiveness of the atherosclerotic process or to guide treatment in the patient with risk factors for atherosclerosis.
Key Words: gene expression oxidative stress atherosclerosis leukocytes
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