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<p>Bisphenol S (BPS) is considered a good substitute for bisphenol A (BPA) in industrial applications, and data suggest that the kidney is an important injury site after BPS exposure. However, the phenotype of kidney injury induced by BPS exposure and the mechanism of its damage remain unknown. Therefore, this study aims to investigate the phenotype and specific mechanism of kidney injury induced by BPS exposure. SD rats are treated with three different doses of BPS (50&#xa0;mg/kg body weight(b.w.), 100&#xa0;mg/kg b.w., and 150&#xa0;mg/ kg b.w.), and HK-2 cells are treated with 100 µM BPS, 200 µM and 400 µM BPS to mimic the in vitro and in vivo environment of BPS exposure-induced kidney injury. Meanwhile, the potential mechanism of BPS exposure-induced kidney injury was screened by RNA sequencing and further verified by in vitro experiments. BPS exposure induces cytoskeletal architecture damage and EMT transformation in HK-2 cells, promoting renal fibrosis. In addition, it was found that activation of the PI3K-AKT-mTOR signaling pathway plays a key role in cytoskeletal architecture damage and EMT transformation in HK-2, and after inhibition of PI3K-AKT-mTOR signaling by Wortmannin, the cytoskeletal architecture disorders, and EMT are partially reversed. In conclusion, we found that the activation of the PI3K-AKT-mTOR signaling pathway can mediate disturbed cytoskeletal architecture and EMT to induce renal fibrosis after BPS exposure.</p>

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The PI3K-AKT-mTOR signaling pathway mediates epithelial mesenchymal transition and cytoskeletal architecture changes induce to renal fibrosis after Bisphenol S exposure

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月5日

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  • Zhaoxia Zhang,
  • Liming Jin,
  • Tao Mi,
  • Jinkui Wang,
  • Zhaoying Wang,
  • Junyi Luo,
  • Chunnian Ren,
  • Xin Wu,
  • Jiayan Liu,
  • Peng Guo,
  • Li Wang,
  • Dawei He

摘要

Bisphenol S (BPS) is considered a good substitute for bisphenol A (BPA) in industrial applications, and data suggest that the kidney is an important injury site after BPS exposure. However, the phenotype of kidney injury induced by BPS exposure and the mechanism of its damage remain unknown. Therefore, this study aims to investigate the phenotype and specific mechanism of kidney injury induced by BPS exposure. SD rats are treated with three different doses of BPS (50 mg/kg body weight(b.w.), 100 mg/kg b.w., and 150 mg/ kg b.w.), and HK-2 cells are treated with 100 µM BPS, 200 µM and 400 µM BPS to mimic the in vitro and in vivo environment of BPS exposure-induced kidney injury. Meanwhile, the potential mechanism of BPS exposure-induced kidney injury was screened by RNA sequencing and further verified by in vitro experiments. BPS exposure induces cytoskeletal architecture damage and EMT transformation in HK-2 cells, promoting renal fibrosis. In addition, it was found that activation of the PI3K-AKT-mTOR signaling pathway plays a key role in cytoskeletal architecture damage and EMT transformation in HK-2, and after inhibition of PI3K-AKT-mTOR signaling by Wortmannin, the cytoskeletal architecture disorders, and EMT are partially reversed. In conclusion, we found that the activation of the PI3K-AKT-mTOR signaling pathway can mediate disturbed cytoskeletal architecture and EMT to induce renal fibrosis after BPS exposure.