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STIM promotes the epithelial-mesenchymal transition of podocytes through regulation of FcγRII activity in diabetic nephropathy.
Histology and Histopathology ( IF 2 ) Pub Date : 2018-11-26 , DOI: 10.14670/hh-18-068
Juan Jin 1, 2 , Meiyu Ye 1, 3 , Kang Hu 1, 3 , Jianguang Gong 1, 2 , Qiang He 1, 2
Affiliation  

Diabetic nephropathy (DN) is a serious complication in diabetic patients and has been considered as the main cause of end-stage renal disease. However, there are no studies on the role of stromal interaction molecule (STIM) and its two subtypes, STIM1 and STIM2, in the epithelial-to-mesenchymal transition (EMT) of podocytes induced by diabetic kidney disease (DKD). The present study suggests for the first time that STIM inhibition decreases DKD-induced EMT.

中文翻译:

STIM通过调节糖尿病性肾病中FcγRII的活性来促进足细胞的上皮-间质转化。

糖尿病肾病(DN)是糖尿病患者的严重并发症,被认为是终末期肾脏疾病的主要原因。然而,尚未有关于间质相互作用分子(STIM)及其两个亚型STIM1和STIM2在糖尿病肾病(DKD)诱导的足细胞上皮-间质转化(EMT)中的作用的研究。本研究首次建议STIM抑制降低DKD诱导的EMT。
更新日期:2020-08-21
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