Byon Chang Hyun, Chen Yabing
Department of Pathology, University of Alabama at Birmingham, 614 Shelby Biomedical Research Bldg., 1825 University Blvd., Birmingham, AL, 35294, USA,
Curr Osteoporos Rep. 2015 Aug;13(4):206-15. doi: 10.1007/s11914-015-0270-3.
Vascular calcification is highly prevalent in patients with chronic kidney disease (CKD) and increases mortality in those patients. Impaired calcium and phosphate homeostasis, increased oxidative stress, and loss of calcification inhibitors have been linked to vascular calcification in CKD. Additionally, impaired bone may perturb serum calcium/phosphate and their key regulator, parathyroid hormone, thus contributing to increased vascular calcification in CKD. Therapeutic approaches for CKD, such as phosphate binders and bisphosphonates, have been shown to ameliorate bone loss as well as vascular calcification. The precise mechanisms responsible for vascular calcification in CKD and the contribution of bone metabolism to vascular calcification have not been elucidated. This review discusses the role of systemic uremic factors and impaired bone metabolism in the pathogenesis of vascular calcification in CKD. The regulation of the key osteogenic transcription factor Runt-related transcription factor 2 (Runx2) and the emerging role of Runx2-dependent receptor activator of nuclear factor kappa-B ligand (RANKL) in vascular calcification of CKD are emphasized.
血管钙化在慢性肾脏病（CKD）患者中极为普遍，并增加了这些患者的死亡率。钙磷稳态受损、氧化应激增加以及钙化抑制剂的丧失与CKD中的血管钙化有关。此外，骨功能受损可能会扰乱血清钙/磷及其关键调节因子甲状旁腺激素，从而导致CKD中血管钙化增加。CKD的治疗方法，如磷结合剂和双膦酸盐，已被证明可改善骨质流失以及血管钙化。CKD中血管钙化的确切机制以及骨代谢对血管钙化的作用尚未阐明。本综述讨论了全身性尿毒症因素和骨代谢受损在CKD血管钙化发病机制中的作用。强调了关键成骨转录因子Runx2相关转录因子2（Runx2）的调节以及Runx2依赖性核因子κB配体受体激活剂（RANKL）在CKD血管钙化中的新作用。
