Review |
From the Bioengineering Department, University of Washington, Seattle, Wash.
Correspondence to Cecilia M. Giachelli, PhD, Professor, Bioengineering, Box 351720, University of Washington, Seattle, WA 98195. E-mail ceci{at}u.washington.edu
This Review is part of a thematic series on Mechanisms of Vascular Calcificiation, which includes the following articles:
The Pathophysiology of Vascular Calcification in Chronic Kidney Disease
Mesenchymal Stem Cells and the Artery Wall
Regulation of Vascular Calcification by Osteoclast Regulatory Factors RANKL and OPG
Regulation of Vascular Calcification: Roles of Phosphate and Osteopontin
Angiogenesis and Pericytes in Initiation of Ectopic Calcification
Role of Bone Morphogenetic Proteins in Vascular Calcification
Linda Demer Guest Editor
Vascular calcification is prevalent in aging as well as a number of pathological conditions, and it is now recognized as a strong predictor of cardiovascular events in the general population as well as diabetic and end-stage renal disease patients. Vascular calcification is a highly regulated process involving inductive and inhibitory mechanisms. This article focuses on two molecules, phosphate and osteopontin, that have been implicated in the induction or inhibition of vascular calcification, respectively. Elevated phosphate is of interest because hyperphosphatemia is recognized as a major nonconventional risk factor for cardiovascular disease mortality in end-stage renal disease patients. Studies to date suggest that elevated phosphate stimulates smooth muscle cell phenotypic transition and mineralization via the activity of a sodium-dependent phosphate cotransporter. Osteopontin, however, appears to block vascular calcification most likely by preventing calcium phosphate crystal growth and inducing cellular mineral resorption.
Key Words: cardiovascular disease osteopontin phosphate pyrophosphate smooth muscle cell vascular calcification
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