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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1331.)
© 2004 American Heart Association, Inc.

Editorials

Aortic Valve

Turning Over a New Leaf(let) in Endothelial Phenotypic Heterogeneity

Peter F. Davies; Anthony G. Passerini; Craig A. Simmons

From the Institute for Medicine and Engineering (P.F.D., A.G.P., C.A.S.), and the Departments of Pathology and Laboratory Medicine (P.F.D.) and Bioengineering (P.F.D., A.G.P., C.A.S.), University of Pennsylvania, Philadelphia, Penn.

Correspondence to Dr Peter F. Davies, Institute for Medicine and Engineering, University of Pennsylvania, 1010 Vagelos Laboratories, 3340 Smith Walk, Philadelphia PA 19104. E-mail pfd@pobox.upenn.edu

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

Aortic valve diseases are debilitating cardiovascular disorders associated with significant morbidity and mortality. Although there continue to be major efforts to improve the longevity of replacement valves and to improve tissue engineered substitutes,¹ the underlying mechanisms that may be responsible for the initiation and development of valve pathology have received less attention than have other sclerosing cardiovascular diseases such as atherogenesis. The endothelium lining of the cardiovascular system plays an important regulatory role in vascular physiology and pathology. In similar fashion, the surfaces of valve leaflets are presumed to be generally protected (eg, anticoagulant) and regulated (eg, permeability) by the endothelium. The functional properties of endothelium or its presence/absence are associated with a variety of valve pathologies,² and systemic endothelial dysfunction is linked to aortic valve calcification.³ However, only recently have cell and molecular studies focused on the characterization of valve endothelial phenotypes with the idea that some aspects of phenotypic change or dysfunction may contribute to valve pathologies, a situation analogous to atherogenesis.

See page 1429

During the cardiac cycle, the aortic valve endothelium is subjected to complex fluid dynamics that are distinctly different on each side of the valve. As has been described for many years, arterial endothelial alignment in vivo generally follows the measured or predicted shear stress direction,⁴ and endothelial cells in vitro align with the dominant direction of the applied shear stress.⁵ The responses, which are reversible,^4,6 represent endothelial structural remodeling in response to hemodynamic shear stress. It might be expected that endothelial cells isolated . . . [Full Text of this Article]

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