The regulation of fibrosis and calcification by gadolinium

肾源性全身性纤维化(NSF)是以严重肾功能不全患者的全身性纤维化和异常钙化为特征。核磁共振成像中使用的含Gd造影剂被认为是NSF的诱因。然而，Gd在NSF中的致病作用和Gd诱导的纤维化和钙化机制尚不清楚。Gd诱导的人骨髓间充质干细胞(MSC)的ET-1/ET受体表达及PDGF受体、ERK和Aktin的磷酸化水平升高，提示Gd可能通过增强ETR信号和/或PDGFR信号以及ERK和Akt信号通路来诱导HMSC的增殖和钙化。

Nephrogenic systemic fibrosis (NSF) is characterized by systemic fibrosis and abnormal calcification in patients with severe renal dysfunction. It is considered that gadolinium (Gd)-containing contrast agents used for magnetic resonance imaging trigger the development of NSF. However, the causative role of Gd and the mechanism of Gd-induced fibrosis and calcification in NSF are unknown. ET-1/ET receptor expression and phosphorylation of PDGF receptor, ERK and Aktin human mesenchymal stem cells (MSC) treated with Gd were elevated, suggeting that Gd induces proliferation and calcification of hMSC via enhancement of ETR signaling and/or PDGFR signaling and ERK and Akt pathway.