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(Hypertension. 2005;46:21.)
© 2005 American Heart Association, Inc.
Editorial Commentaries |
From the Center for the Study of Sex Differences in Health, Aging and Disease, Georgetown University, Washington DC.
Correspondence to Kathryn Sandberg, PhD, Director, Center for the Study of Sex Differences in Health, Aging and Disease; Professor of Medicine and Physiology at Georgetown University. Suite 232 Building D, 4000 Reservoir Road, NW. Washington, DC 20057. E-mail sandberg@georgetown.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Over the past decade, inflammation has been gaining widespread attention among scientists because of accumulating evidence implicating inflammation as an important mediator in the progression of cardiovascular disease (CVD). Clinical and experimental studies have shown strong associations between the risk for CVD and several inflammatory markers. In the majority of conditions that are high risk factors for CVD (eg, hypercholesterolemia, hypertension, and diabetes), the vascular system or, more specifically, the vascular endothelium, elicits an inflammatory response that could lead to increased oxidative stress as well as to other processes that contribute to vascular damage.1 This theory has also been supported by the fact that the most common drugs used for the treatment of CVDstatins, aspirin, angiotensin II inhibitors, and PPAR
agonistsall have anti-inflammatory effects. Among the proinflammatory molecules, tumor necrosis factor-
(TNF-
) has been identified as an important mediator of vascular dysfunction through its ability to decrease the expression of endothelial nitric oxide synthase (eNOS)2 and, concomitantly, to induce NAD(P)H oxidase activity.3 Moreover, high levels of TNF-
in the systemic circulation have been detected in conditions that present significant risk for CVD such as hypertension and diabetes.4 In this issue, Arenas et al5 demonstrate a new role of TNF-
in the development of vascular dysfunction in what can be considered another risk factor for CVD, ie, estrogen deficiency.
Although heated controversy exists over the value of estrogen replacement therapy in protecting against cardiovascular disease, many animal and clinical studies have shown that estrogen has direct beneficial effects on the
Related Article:
Inhibition Enhances NO Modulation of Vascular Function in Estrogen-Deficient Rats
Hypertension 2005 46: 76-81.
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