Zhao Yunyun, Sun Zhen, Li Lihua, Yuan Wei, Wang Zhongqun
Departments of Cardiology; and.
Pathology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
J Cardiovasc Pharmacol. 2022 Dec 1;80(6):769-778. doi: 10.1097/FJC.0000000000001359.
Vascular calcification is a pathological process characterized by ectopic calcification of the vascular wall. Medial calcifications are most often associated with kidney disease, diabetes, hypertension, and advanced age. Intimal calcifications are associated with atherosclerosis. Collagen can regulate mineralization by binding to apatite minerals and promoting their deposition, binding to collagen receptors to initiate signal transduction, and inducing cell transdifferentiation. In the process of vascular calcification, type I collagen is not only the scaffold for mineral deposition but also a signal entity, guiding the distribution, aggregation, and nucleation of vesicles and promoting the transformation of vascular smooth muscle cells into osteochondral-like cells. In recent years, collagen has been shown to affect vascular calcification through collagen disc-domain receptors, matrix vesicles, and transdifferentiation of vascular smooth muscle cells.
血管钙化是一种以血管壁异位钙化为特征的病理过程。中层钙化最常与肾脏疾病、糖尿病、高血压和高龄相关。内膜钙化与动脉粥样硬化有关。胶原蛋白可通过与磷灰石矿物质结合并促进其沉积、与胶原蛋白受体结合以启动信号转导以及诱导细胞转分化来调节矿化。在血管钙化过程中，I型胶原蛋白不仅是矿物质沉积的支架，也是一种信号实体，引导囊泡的分布、聚集和成核，并促进血管平滑肌细胞向骨软骨样细胞转化。近年来，已表明胶原蛋白可通过胶原蛋白盘状结构域受体、基质囊泡和血管平滑肌细胞的转分化来影响血管钙化。
