文献类型：期刊文献

英文题名：MiR-192-5p protects hexavalent chromium-induced apoptosis in renal epithelial cells by inhibiting p53 signaling pathway

作者：Wen, Leying[1];Cai, Kai[1];Fan, Caixia[1];Jin, Lifang[1,2];Fu, Guoquan[1,2];Yan, Junyan[1]

机构：[1]Shaoxing Univ, Sch Life & Environm Sci, Shaoxing 312000, Zhejiang, Peoples R China;[2]Hangzhou Hongwang Med Lab Co Ltd, Hangzhou 310000, Zhejiang, Peoples R China

年份：2025

外文期刊名：MOLECULAR & CELLULAR TOXICOLOGY

收录：SCI-EXPANDED(收录号：WOS:001513448500001)、、Scopus(收录号：2-s2.0-105008762603)、WOS

基金：This work was supported by research grants from the Natural Science Foundation of Zhejiang Province (NO. LQ20B070003).

语种：英文

外文关键词：Hexavalent chromium Cr(VI); miR-192-5p; Apoptosis; p53 pathway; HK-2 cells

外文摘要：BackgroundExposure to hexavalent chromium [Cr(VI)] is recognized to be nephrotoxic, accompanied by alterations in the blood exosomal microRNA (miRNA) profile. Despite this association, the specific regulatory roles of exosomal miRNAs in Cr(VI)-induced kidney injury remain unknown.ObjectiveTo explore exosomal miRNA expression variations in blood exposed to Cr(VI) and their potential effects on Cr(VI)-exposed renal epithelial cells.ResultsExposure to Cr(VI) caused nephrotoxicity in mice. Notably, significant changes in the expression of specific exosomal miRNAs were observed, including a marked up-regulation of miR-192-5p in Cr(VI)-exposed mouse blood. Experiments using HK-2 renal tubular epithelial cells demonstrated that miR-192-5p treatment alleviated Cr(VI)-induced cytotoxicity by reducing apoptosis. Further, it was revealed that miR-192-5p suppressed the p53 signaling pathway, inhibiting apoptosis while promoting cell cycle arrest.ConclusionmiR-192-5p attenuated Cr(VI)-induced renal epithelial cytotoxicity via indirectly modulating the p53 signaling cascade. This study advances our understanding of the molecular mechanisms behind Cr(VI)-induced renal injury and identifies miR-192-5p as a viable target for intervention to mitigate kidney damage caused by toxic metal exposure.