Chen Neal X, Moe Sharon M
Department of Medicine, Indiana University School of Medicine, 950 W. Walnut Street, R2-202, Indianapolis, IN, 46202, USA.
Department of Anatomy and Cell Biology, Indiana University School of Medicine, 950 W. Walnut Street, R2-202, Indianapolis, IN, 46202, USA.
Curr Osteoporos Rep. 2015 Dec;13(6):372-80. doi: 10.1007/s11914-015-0293-9.
Vascular calcification can lead to cardiovascular morbidity and mortality. The initiating factors and clinical consequences depend on the underlying disease state and location of the calcification. The pathogenesis of vascular calcification is complex and involves a transformation of vascular smooth muscle cells to an osteo/chondrocytic cell that expresses RUNX2 and produces matrix vesicles. The imbalance of promoters (such as hyperphosphatemia and hypercalcemia) and inhibitors (e.g., fetuin-A) is critical in the development of vascular calcification. The altered mineral metabolism and deficiency in inhibitors are common in patients with chronic kidney disease (CKD) and is one reason why vascular calcification is so prevalent in that population.
血管钙化可导致心血管疾病的发病率和死亡率。引发因素和临床后果取决于潜在的疾病状态以及钙化的位置。血管钙化的发病机制复杂,涉及血管平滑肌细胞向表达RUNX2并产生基质小泡的骨/软骨细胞转变。促进因子(如高磷血症和高钙血症)和抑制因子(如胎球蛋白-A)的失衡在血管钙化的发展过程中至关重要。矿物质代谢改变和抑制因子缺乏在慢性肾脏病(CKD)患者中很常见,这也是该人群中血管钙化如此普遍的原因之一。