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首页> 外文期刊>Journal of cellular physiology. >Identification of YAP1 as a novel downstream effector of the FGF2/STAT3 pathway in the pathogenesis of renal tubulointerstitial fibrosis
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Identification of YAP1 as a novel downstream effector of the FGF2/STAT3 pathway in the pathogenesis of renal tubulointerstitial fibrosis

机译:下游YAP1作为小说的识别FGF2 / STAT3通路的效应阻力指标纤维化也许可以肾的发病机理

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摘要

Chronic kidney disease is a global health problem and eventually develops into an end-stage renal disease (ESRD). It is now widely believed that renal tubulointerstitial fibrosis (TIF) plays an important role in the progression of ESRD. Renal tubular epithelial-mesenchymal transition (EMT) is an important cause of TIF. Studies have shown that FGF2 is highly expressed in fibrotic renal tissue, although the mechanism remains unclear. We found that FGF2 can activate STAT3 and induce EMT in renal tubular epithelial cells. STAT3, an important transcription factor, was predicted by the JASPAR biological database to bind to the promoter region of YAP1. In this study, STAT3 was shown to promote the expression of the downstream target gene YAP1 through transcription, promote EMT of renal tubular epithelial cells, and mediate the occurrence of renal TIF. This study provides a theoretical basis for the involvement of the FGF2/STAT3/YAP1 signaling pathway in the process of renal interstitial fibrosis and provides a potential target for the treatment of renal fibrosis.
机译:慢性肾脏疾病是一个全球性的健康问题并最终发展为终末期肾疾病(ESRD)。阻力指标纤维化也许可以肾(TIF)扮演在ESRD的发展中扮演着重要角色。管状epithelial-mesenchymal过渡(EMT)气管无名动脉瘘管的是一个重要的原因。FGF2纤维化肾中高度表达组织,但机制尚不清楚。我们发现FGF2可以激活STAT3和诱导EMT在肾小管上皮细胞。重要的转录因子,预测了绑定到JASPAR生物数据库YAP1的启动子区域。促进下游的表达式目标基因通过转录YAP1,促进EMT的肾小管上皮细胞气管无名动脉瘘管的调解肾的发生。参与提供了理论依据FGF2 / STAT3 / YAP1信号通路肾间质纤维化和过程提供了一个潜在的治疗目标肾纤维化。

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