Pin1通过抑制Wnt/β-catenin信号参与CKD-MBD的发病

慢性肾脏病-矿物质和骨异常（CKD-MBD）是慢性肾脏病（CKD）常见并发症之一。近年研究表明骨代谢异常在CKD早期即已出现，是CKD-MBD发生发展的中心环节。而骨细胞特异性Wnt/β-catenin信号的异常是造成CKD骨代谢紊乱的重要机制。肽酰脯氨酰胺同分异构酶（Pin1）依赖的磷酸化丝/苏-脯氨基酸基序异构是调控Wnt/β-catenin信号通路的重要途径，Pin1的调节异常能够改变Wnt/β-catenin信号的作用，可能参与CKD MBD的进展。本文旨在探讨Pin1通过抑制Wnt/β-catenin信号参与CKD-MBD的发病。

Pin1 Contributes to CKD MBD by derepression of Wnt/β-catenin signaling

Chronic kidney disease-mineral and bone disorder(CKD-MBD) is one of the common complications of chronic kidney disease. Recent studies had shown that bone metabolism abnormalities had emerged in the early stages of CKD and were central to the development of CKD-MBD. The abnormality of bone cell specific Wnt/β-catenin signaling was an important mechanism of CKD bone metabolic abnormalities. Peptidyl-proplyl cis/trans isomerase 1(Pin1)-dependent phosphorylation of Ser/Thr.Pro motifs isomerism is an important pathway for the regulation of Wnt/β-catenin signaling. Impaired regulation of Pin1 can alter the role of Wnt/β-catenin signaling and may be involved in the progression of CKD-MBD.The article aims to investigate the role of Pin1 in the pathogenesis of CKD-MBD by inhibiting Wnt/β-catenin signaling