Van Campenhout Ann, Golledge Jonathan
Vascular Biology Unit, Department of Surgery, School of Medicine, James Cook University, Townsville, QLD 4811, Australia.
Atherosclerosis. 2009 Jun;204(2):321-9. doi: 10.1016/j.atherosclerosis.2008.09.033. Epub 2008 Oct 9.
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.
骨病理学与动脉粥样硬化之间的关联促使人们寻找连接骨骼系统和血管系统的共同介质。自最初被发现是骨代谢的关键调节因子以来，骨保护素（OPG）因其在血管疾病和钙化中的作用而成为人们密切关注的对象。体外研究和动物模型研究表明，OPG可抑制血管钙化。然而，矛盾的是，临床研究表明，血清OPG水平会随着血管钙化、冠状动脉疾病、中风及未来心血管事件的发生而升高。这引发了关于OPG作为血管疾病生物标志物潜力的广泛争论。然而，这种骨调节蛋白影响心血管病理生理学的确切意义和机制仍不清楚。越来越多有价值的研究表明，OPG不仅是一种标志物，还是调节成骨、炎症和凋亡反应的血管病理介质，这满足了人们对更全面认识的需求。通过整合近期实验研究、动物模型和临床研究的结果，本综述总结了目前对OPG在血管疾病和钙化中作用的认识。
