论文部分内容阅读
动脉钙化是糖尿病、动脉粥样硬化及慢性肾功能衰竭等疾病的共同病理过程,目前认为动脉钙化形成的早期过程是一个与骨发育相似的主动的、可预防、可逆转的高度可调控的生物学过程。动脉中膜钙化发生的中心环节是血管平滑肌细胞(VSMC)向成骨样细胞的转分化,VSMC在诱导条件下可转变为成骨样细胞,并合成和分泌多种骨形成蛋白。因此,成骨细胞的诱导、抑制钙化的有关因子缺失都可导致动脉中膜钙化。目前研究表明,晚期糖基化终末产物及其受体以及Wnt/β-连环蛋白信号通路都与VSMC的表型转化、动脉中膜钙化过程有着密切的联系,但其具体分子途径尚待继续探究。
Arterial calcification is a common pathological process of diseases such as diabetes, atherosclerosis and chronic renal failure. At present, it is thought that the early process of arterial calcification is an active, preventable and reversible highly-regulated organism similar to bone development Learn process. The central part of arterial calcification is the transdifferentiation of vascular smooth muscle cells (VSMCs) to osteoblast-like cells. VSMCs can transform into osteoblast-like cells under induction and synthesize and secrete a variety of bone morphogenic proteins. Therefore, the induction of osteoblasts and the loss of relevant factors that inhibit calcification can lead to calcification of the artery. Recent studies have shown that both advanced glycation end products and their receptors as well as the Wnt / β-catenin signaling pathway are closely related to the phenotypic transformation of VSMC and the process of arterial intimal calcification, but the specific molecular pathways to be continued Explore.