Department of Bioengineering, University of Washington, Box 355061, Seattle, WA, 98195, USA.
Calcif Tissue Int. 2013 Oct;93(4):365-73. doi: 10.1007/s00223-013-9712-z. Epub 2013 Mar 1.
Vascular calcification is highly associated with cardiovascular disease mortality, particularly in high-risk patients with diabetes and chronic kidney diseases (CKD). In blood vessels, intimal calcification is associated with atherosclerosis, whereas medial calcification is a nonocclusive process which leads to increased vascular stiffness and reduced vascular compliance. In the valves, calcification of the leaflets can change the mechanical properties of the tissue and result in stenosis. For many decades, vascular calcification has been noted as a consequence of aging. Studies now confirm that vascular calcification is an actively regulated process and shares many features with bone development and metabolism. This review provides an update on the mechanisms of vascular calcification including the emerging roles of the RANK/RANKL/OPG triad, osteoclasts, and microRNAs. Potential treatments adapted from osteoporosis and CKD treatments that are under investigation for preventing and/or regressing vascular calcification are also reviewed.
血管钙化与心血管疾病死亡率高度相关,尤其是在患有糖尿病和慢性肾脏病 (CKD) 的高危患者中。在血管中,内膜钙化与动脉粥样硬化有关,而中膜钙化是一种非阻塞性过程,可导致血管僵硬增加和血管顺应性降低。在瓣膜中,瓣叶的钙化会改变组织的机械性能,导致狭窄。几十年来,血管钙化一直被认为是衰老的结果。现在的研究证实,血管钙化是一个受调控的过程,它与骨骼发育和代谢有许多共同特征。这篇综述提供了血管钙化机制的最新信息,包括 RANK/RANKL/OPG 三联体、破骨细胞和 microRNAs 的新作用。还回顾了正在研究用于预防和/或逆转血管钙化的骨质疏松症和 CKD 治疗的潜在治疗方法。