doi: 10.1161/01.RES.0000163634.51301.0d
© 2005 American Heart Association, Inc.
Reviews |
Angiogenesis and Pericytes in the Initiation of Ectopic Calcification
From the Wellcome Trust Centre for Cell-Matrix Research & Cardiovascular Research Group, Faculty of Medical & Human Sciences, University of Manchester, Manchester M13 9PT, UK.
Correspondence to Dr A.E. Canfield, University of Manchester, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK, Tel: +44 161 275 5066, Fax: +44 161 275 5082, E-mail ann.canfield{at}manchester.ac.uk
This Review is part of a thematic series on Mechanisms of Vascular Calcification, 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
Role of Bone Morphogenetic Proteins in Vascular Calcification
Angiogenesis and Pericytes in the Initiation of Ectopic Calcification
Osteopontin Promoter Regulation and Phosphate Transport Molecules in Vascular Calcification
Linda Demer Guest Editor
Ectopic calcification of blood vessels, heart valves, and skeletal muscle is a major clinical problem. There is now good evidence that angiogenesis is associated with ectopic calcification in these tissues and that it is necessary, but not sufficient, for calcification to occur. Angiogenesis may regulate ectopic calcification in several ways. First, many angiogenic factors are now known to exert both direct and indirect effects on bone and cartilage formation. Second, cytokines released by endothelial cells can induce the differentiation of osteoprogenitor cells. Third, the new blood vessels provide oxygen and nutrients to support the growing bone. Finally, the new blood vessels can serve as a conduit for osteoprogenitor cells. These osteoprogenitor cells may be derived from the circulation or from pericytes that are present in the neovessels themselves. Indeed, there is now compelling evidence that pericytes can differentiate into osteoblasts and chondrocytes both in vitro and in vivo. Other vascular cells, including adventitial myofibroblasts, calcifying vascular cells, smooth muscle cells, and valvular interstitial cells, have also been shown to exhibit multilineage potential in vitro. Although these cells share many properties with pericytes, the precise relationship between them is not known. Furthermore, it still remains to be determined whether all or some of these cells contribute to the ectopic calcification observed in vivo. A better understanding of the underlying mechanisms that link angiogenesis, pericytes, and ectopic calcification should provide a basis for development of therapeutic strategies to treat or arrest this clinically significant condition.
Key Words: pericytes • angiogenesis • calcification • atherosclerosis • smooth muscle cells
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