慢性肾脏病血管钙化的分子机制研究进展

Research progress on molecular mechanism of vascular calcification in chronic kidney disease

矿物质代谢紊乱导致慢性肾脏病(CKD)患者血管平滑肌细胞(VSMC)的成骨样转分化,而钙化促进及抑制因子的调控失衡又促进了血管钙化。本篇主要围绕钙化促进因子Runt相关转录因子2(Runx2)及T细胞死亡相关基因51(TDAG51)参与血管钙化的机制进行综述。

Disorders of mineral metabolism lead to osteogenic transdifferentiation of vascular smooth muscle cells(VSMC)in patients with chronic kidney disease(CKD),and the unbalanced regulation of promotion and inhibitory factors for calcification leads to vascular calcification.This review mainly focused on the vascular calcification mechanism in which the calcification-promoting factor Runt-related transcription factor 2(Runx2)and T-cell death-associated gene 51(TDAG51)were involved.