LncRNA KCNQ1OT1 (potassium voltage-gated channel subfamily Q member 1 opposite strand/antin transcript 1) aggravates acute kidney injury by activating p38/NF-κB pathway via miR-212-3p/MAPK1 (mitogen-activated protein
安全知识大全kina 1) axis in psis
期刊名称： Bioengineered猫图片头像
作者： Changhua Liu,Bo Gao,Xiaolan Xu,Gang Zhou,Haixia Wang,Hongbin Mou 作者机构： Department of Nephrology, Subei Peoples Hospital of Jiangsu
五指山图片
Province, Yangzhou, China,Department of Critical Care Medicine, Subei Peoples Hospital of Jiangsu Province, Yangzhou, China
年份： 2021年
期号： 第2期繁转简
夹心木
什么是排畸检查关键词： Acute kidney injury;MAPK1;KCNQ1OT;p38/nf-κB;ceRNA北京摇号申请
摘要：Acute kidney injury (AKI), a common complication of psis, is characterized by a rapid loss of renal excretory function. A variety of etiologies and pathophysiological process may contribute to AKI. Previously, mitogen-activated protein kina 1 (MAPK1) was reported to regulate cellular process in various psis-associated dias. The current study aimed to further explore the biological function and regulatory mechanism of MAPK1 in psis-induced AKI. In our study, MAPK1 exhibited high expression in the rum of AKI patients. Functionally, knockdown of MAPK1 suppresd inflammatory respon, cell apoptosis in respon of lipopolysaccharide (LPS) induction in HK-2 cells. Moreover, MAPK1 deficiency alleviated renal inflammation, renal dysfunction, and renal injury in vivo . Mechanistically, MAPK1 could activate
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