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Regulation of Fn14 stability by scF~Fbxw7alpha during septic acute kidney injury

机译:scF~Fbxw7alpha在脓毒性急性肾损伤过程中对Fn14稳定性的调控

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摘要

Acute kidney injury (AKI) initiated by sepsis remains a thorny problem despite recent advancements in its clinical management. Having been found to be activated during AKI, fibro-blast growth factor-inducible molecule 14 (Fnl4) may be a potential therapeutic target because of its involvement in the molecular basis of injury. Here, we report that LPS induces apoptosis of mouse cortical tubule cells mediated by Fn14, for which simultaneous Toll-like receptor (TLR)4 activation is required.
机译:脓毒症引发的急性肾损伤 (AKI) 仍然是一个棘手的问题,尽管其临床管理最近取得了进展。已发现在 AKI 期间被激活,纤维原始生长因子诱导分子 14 (Fnl4) 可能是一个潜在的治疗靶点,因为它参与损伤的分子基础。在这里,我们报道LPS诱导由Fn14介导的小鼠皮质小管细胞凋亡,需要同时激活Toll样受体(TLR)4。

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