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(Circulation Research. 2007;100:1405.)
© 2007 American Heart Association, Inc.

Editorials

C-Reactive Protein and Reendothelialization

NO Involvement

Paul E. Szmitko, Subodh Verma

From the Division of Cardiac Surgery, St. Michael’s Hospital (S.V.) and the Division of General Internal Medicine (P.E.S.), University of Toronto, Canada.

Correspondence to Subodh Verma, MD, PhD, Division of Cardiac Surgery, Suite 8–003F, Bond Wing, St. Michael’s Hospital, 30 Bond Street, Toronto, Ontario, Canada, M5B 1W8. E-mail subodh.verma@sympatico.ca

See related article, pages 1452–1459

Key Words: Key Words: • C-reactive protein • nitric oxide • reendothelialization

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

Disruption of the endothelium and its subsequent dysfunction appears to set the stage for atherogenesis.¹ The maintenance of vascular homeostasis depends in part on a balance between endothelium-derived relaxing and contracting factors. Alterations in this balance lead to inflammation and the formation of fatty streaks and fibrous plaques. The diminished production or availability of nitric oxide (NO) appears paramount to setting the stage for inflammation and vascular injury.

In addition to its vasodilatory effect on the vasculature, endothelium-derived NO promotes endothelial cell growth, survival and migration,² stimulates angiogenesis and neovascularization in part by endothelial progenitor cell (EPC) recruitment,³ inhibits leukocyte adhesion to the endothelium,⁴ maintains vascular smooth muscle in a nonproliferative state,⁵ and limits platelet aggregation and thrombosis.⁶ Maintenance of an intact and functional endothelium protects against vascular disease while its disruption is detrimental. The study by Schwartz et al,⁷ in this issue of Circulation Research, adds to our understanding of how C-reactive protein (CRP) works to promote vascular pathology by inhibiting NO synthesis.

CRP, long regarded as an acute phase protein and an active participant in the innate immune system, has more recently been linked to the development of cardiovascular disease.⁸ On the basis of several prospective epidemiologic studies, circulating high sensitivity CRP has emerged as an independent predictor of cardiovascular disease risk in various subgroups of patients, including those without overt cardiovascular disease, patients with stable angina or acute coronary syndromes, and in those with the metabolic syndrome.^9–12 In primary prevention, CRP confers additional prognostic value at . . . [Full Text of this Article]