检索历史 清除

慢性肾脏病（chronic kidney disease，CKD）患者体内长期处于低氧状态，低氧诱导因子（hypoxia inducible factor，HIF）作为调控低氧反应的关键调节因子，不仅可以通过多种信号传导通路表达分泌多种成骨标志物，促进血管平滑肌细胞（vascular smooth muscle cells，VSMCs）成骨样分化，参与血管钙化（vascular calcification，VC）形成，还可通过诱导氧化应激、细胞自噬及参与糖酵解途径等途径参与VC，极大提升CKD患者心血管事件发病率和病死率。本文将从低氧状态下HIF引发CKD患者VC的作用机制及可能的治疗方法对CKD患者VC相关研究进行综述。

Patients with chronic kidney disease are in a state of hypoxia for a long time. Hypoxia-inducible factor, as a key regulator of the hypoxia response, can regulate the expression and secretion of various osteogenic markers through multiple signaling pathways, promote osteogenic differentiation of vascular smooth muscle cells,and participate in the formation of vascular calcification. It can also contribute to vascular calcification by inducing oxidative stress, promoting autophagy, and influencing the glycolysis pathway. This involvement significantly increases the morbidity and mortality associated with cardiovascular events in patients with chronic kidney disease. This article reviews the research related to the mechanisms of vascular calcification in patients with chronic kidney disease induced by hypoxia-inducible factor under hypoxic conditions, as well as the possible treatments for this disease.