Journal
ATHEROSCLEROSIS
Volume 204, Issue 2, Pages 321-329Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2008.09.033
Keywords
Osteoprotegerin; Vascular disease; Calcification; Inflammation; Apoptosis
Funding
- National Institute of Health, USA [RO1 HL080010-01]
- National, Health and Medical Research Council, Australia [540405]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL080010] Funding Source: NIH RePORTER
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The association of bone pathologies with atherosclerosis has stimulated the search for common mediators linking the skeletal and the vascular system. Since its initial discovery as a key regulator in bone metabolism, osteoprotegerin (OPG) has become the subject of intense interest for its role in vascular disease and calcification. Studies in vitro and in animal models suggest that OPG inhibits vascular calcification. Paradoxically however, clinical studies suggest that serum OPG levels increase in association with vascular calcification, coronary artery disease, stroke and future cardiovascular events. This has led to an extensive debate on the potential of OPG as a biomarker of vascular disease. However the exact significance and mechanisms by which this bone-regulatory protein influences cardiovascular pathophysiology is still unclear. The need for a more complete picture is being addressed in increasing valuable research indicating OPG as not only a marker but also a mediator of vascular pathology modulating osteogenic, inflammatory and apoptotic responses. By integrating the results of recent experimental research, animal models and clinical studies, this review summarises the present understanding of the role of OPG in vascular disease and calcification. (C) 2008 Elsevier Ireland Ltd. All rights reserved
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