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Kidney injury molecule-1 (KIM-1) mediates renal epithelial cell repair via ERK MAPK signaling pathway

机译:肾损伤分子1(KIM-1)通过ERK MAPK信号通路介导肾上皮细胞修复

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摘要

The expression of kidney injury molecule-1 (KIM-1), a very promising sensitive and specific urinary biomarker for acute renal injury, is markedly upregulated in injured and regenerating renal proximal tubular epithelial cells following ischemic or toxic insults, suggesting a possible role for this molecule in renal repair process. In the present study we report that expression of KIM-1 facilitates renal tubular epithelial cell repair by promoting cell migration and proliferation. KIM-1 expression also enhances ERK MAPK activation, and the modulatory effect of KIM-1 on cellular repair process is likely mediated via ERK MAPK signaling pathway.
机译:肾损伤分子1(KIM-1)的表达是急性肾损伤的非常有希望的敏感和特异性尿生物标志物,在缺血或毒性损伤后受损和再生的肾近端肾小管上皮细胞中表达明显上调,提示其可能的作用。该分子在肾脏修复过程中。在本研究中,我们报道了KIM-1的表达通过促进细胞迁移和增殖而促进了肾小管上皮细胞的修复。 KIM-1表达还增强ERK MAPK激活,并且KIM-1对细胞修复过程的调节作用可能是通过ERK MAPK信号传导途径介导的。

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