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Background <p>Exposure 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.</p> Objective <p>To explore exosomal miRNA expression variations in blood exposed to Cr(VI) and their potential effects on Cr(VI)-exposed renal epithelial cells.</p> Results <p>Exposure 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.</p> Conclusion <p>miR-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.</p>

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

  • 期刊论文

  • 发表日期：

    2025年6月23日

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  • Leying Wen,
  • Kai Cai,
  • Caixia Fan,
  • Lifang Jin,
  • Guoquan Fu,
  • Junyan Yan

摘要

Background

Exposure 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.

Objective

To explore exosomal miRNA expression variations in blood exposed to Cr(VI) and their potential effects on Cr(VI)-exposed renal epithelial cells.

Results

Exposure 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.

Conclusion

miR-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.