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<p>Ischemia–reperfusion injury (I/R), a leading cause of acute kidney injury (AKI) and often progressing to chronic kidney disease (CKD), is characterized by fibrotic changes in kidney parenchyma. Estrogen exerts reno-protective effects through estrogen receptors, but the specific role of estrogen receptor β (ERβ) remains unclear. Therefore, this study aims to investigate the effects of diarylpropionitrile (DPN), a selective ERβ agonist, on kidney I/R injury and subsequent fibrosis in mice. DPN administration prevented increases in plasma creatinine and blood urea nitrogen, tubular damage, and oxidative stress following bilateral kidney I/R. DPN enhanced extracellular signal-regulated kinase 1/2 (ERK) activation and promoted tubular cell proliferation after kidney I/R. Additionally, DPN administration inhibited I/R-induced increases in interstitial expansion, collagen deposition, and expression of vimentin and α-smooth muscle actin. In contrast, DPN enhanced the proliferation of tubular epithelial cells after kidney I/R. Collectively, these findings indicate that DPN protects the kidney from I/R injury and inhibits fibrotic development, suggesting that ERβ may be considered as a potential therapeutic target for treating AKI and CKD.</p>

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Diarylpropionitrile, a selective agonist of estrogen receptor β, protects the kidney against ischemia–reperfusion injury and enhances the repair of tubular epithelial cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月9日

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  • Yong Kwon Han,
  • GiBong Jang,
  • You Ri Park,
  • Hui Jae Lim,
  • Kwon Moo Park

摘要

Ischemia–reperfusion injury (I/R), a leading cause of acute kidney injury (AKI) and often progressing to chronic kidney disease (CKD), is characterized by fibrotic changes in kidney parenchyma. Estrogen exerts reno-protective effects through estrogen receptors, but the specific role of estrogen receptor β (ERβ) remains unclear. Therefore, this study aims to investigate the effects of diarylpropionitrile (DPN), a selective ERβ agonist, on kidney I/R injury and subsequent fibrosis in mice. DPN administration prevented increases in plasma creatinine and blood urea nitrogen, tubular damage, and oxidative stress following bilateral kidney I/R. DPN enhanced extracellular signal-regulated kinase 1/2 (ERK) activation and promoted tubular cell proliferation after kidney I/R. Additionally, DPN administration inhibited I/R-induced increases in interstitial expansion, collagen deposition, and expression of vimentin and α-smooth muscle actin. In contrast, DPN enhanced the proliferation of tubular epithelial cells after kidney I/R. Collectively, these findings indicate that DPN protects the kidney from I/R injury and inhibits fibrotic development, suggesting that ERβ may be considered as a potential therapeutic target for treating AKI and CKD.