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SUN-048 Endothelial STC1 prevents Lipopolysaccharide-induced actue kidney injury via TGF beta

机译:Sun-048内皮STC1通过TGFβ可防止脂多糖诱导的急性肾损伤

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Introduction: Lipopolysaccharide (LPS)-induced Epithelial injury plays acritical role in the pathogenesis of acute kidney injury (AKI). Stannio-calcin-1 (STC1), a pleiotropic glycoprotein, has been reported to protectischemic renal injury by reducing redox oxygen species, modulating in-flammatory release, and inhibiting cell apoptosis. However, regulators ofSTC1 expression as well as its physiologic function in kidneys were un-known. We sought to elucidate the relationship between TGF b and STC1in LPS-induced kidney injury in vitro and in vivo and to define thefunctional role of STC1 expression in renal tubular epithelium.
机译:介绍:脂多糖(LPS)诱导的上皮损伤在急性肾损伤(AKI)发病机制中发挥响应作用。据据报道,Stannio-calcin-1(STC1),脂肪蛋白是通过减少氧化还原氧物种,调节灼热释放和抑制细胞凋亡来保护肾损伤。然而,USSTC1表达的调节剂以及其在肾脏中的生理功能是无名的。我们试图阐明TGF B和STC1在体外和体内肾损伤之间的关系,并在体内确定STC1表达在肾小管上皮中的功能作用。

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