肾损伤分子-1（KIM-1）通过ERK丝裂原活化蛋白激酶信号通路介导肾上皮细胞修复。
Kidney injury molecule-1 (KIM-1) mediates renal epithelial cell repair via ERK MAPK signaling pathway.
作者信息
Zhang Zhiwei, Cai Cindy X
机构信息
Division of Nephrology, Department of Medicine, VA Loma Linda Healthcare System (111 N) and Loma Linda University School of Medicine, 11201 Benton Street, Loma Linda, CA, 92357, USA.
Division of Gastroenterology, Department of Medicine, VA Loma Linda Healthcare System and Loma Linda University School of Medicine, Loma Linda, CA, USA.
出版信息
Mol Cell Biochem. 2016 May;416(1-2):109-16. doi: 10.1007/s11010-016-2700-7. Epub 2016 Apr 15.
Abstract
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.
摘要
肾损伤分子-1（KIM-1）是一种极具前景的急性肾损伤敏感且特异的尿液生物标志物，在缺血或毒性损伤后受损及再生的肾近端小管上皮细胞中，其表达显著上调，提示该分子在肾脏修复过程中可能发挥作用。在本研究中，我们报告KIM-1的表达通过促进细胞迁移和增殖来促进肾小管上皮细胞修复。KIM-1的表达还增强了ERK MAPK的激活，并且KIM-1对细胞修复过程的调节作用可能是通过ERK MAPK信号通路介导的。
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