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<p>Acute kidney injury (AKI) is a clinical syndrome characterized by a rapid decline in glomerular filtration function caused by multiple factors. Factors such as stones and tumors can lead to AKI following renal obstruction. Renal tubular epithelial cell injury is a key component of the pathophysiological mechanism of ischemic acute kidney injury after obstruction.Oxygen–glucose deprivation (OGD) in HK-2 cells and a mouse model of unilateral ureteral ligation (UUO) were used to investigate the role of Claudin-2 in renal tubular epithelial cell apoptosis in ischemia-induced AKI.&#xa0;In animal experiments, the expression of Claudin-2 protein was decreased, while Bax and Caspase-3 expression were increased, and Bcl-2 expression was decreased in the renal tissue of UUO mice. Similarly, after OGD treatment, Claudin-2 protein expression was decreased, Bax and Caspase-3 expression were increased, and Bcl-2 expression was decreased. Upregulation of Claudin-2 protein expression through lentivirus transfection in OGD-treated HK-2 cells reduced the decline in cell viability and the proportion of apoptotic cells. Additionally, upregulation of Claudin-2 protein expression reduced OGD-induced Caspase-3 expression, while the Bax/Bcl-2 ratio showed no significant change. The expression of Claudin-2 is decreased during acute obstructive kidney injury, which contributes to changes in Caspase-3 apoptotic protein and activates cell apoptosis,while the Bax/Bcl-2 ratio showed no significant change.Claudin-2 protein likely modulates apoptosis through a caspase-3-dependent pathway independent of the Bax/Bcl-2 ratio.</p>

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Mechanism of claudin-2 in RTECs apoptosis after renal obstruction

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月2日

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  • Dongsheng zhao,
  • Guijiang Tang,
  • Guoqian Hu,
  • Liang Zeng,
  • Wen Su,
  • Jin Tang

摘要

Acute kidney injury (AKI) is a clinical syndrome characterized by a rapid decline in glomerular filtration function caused by multiple factors. Factors such as stones and tumors can lead to AKI following renal obstruction. Renal tubular epithelial cell injury is a key component of the pathophysiological mechanism of ischemic acute kidney injury after obstruction.Oxygen–glucose deprivation (OGD) in HK-2 cells and a mouse model of unilateral ureteral ligation (UUO) were used to investigate the role of Claudin-2 in renal tubular epithelial cell apoptosis in ischemia-induced AKI. In animal experiments, the expression of Claudin-2 protein was decreased, while Bax and Caspase-3 expression were increased, and Bcl-2 expression was decreased in the renal tissue of UUO mice. Similarly, after OGD treatment, Claudin-2 protein expression was decreased, Bax and Caspase-3 expression were increased, and Bcl-2 expression was decreased. Upregulation of Claudin-2 protein expression through lentivirus transfection in OGD-treated HK-2 cells reduced the decline in cell viability and the proportion of apoptotic cells. Additionally, upregulation of Claudin-2 protein expression reduced OGD-induced Caspase-3 expression, while the Bax/Bcl-2 ratio showed no significant change. The expression of Claudin-2 is decreased during acute obstructive kidney injury, which contributes to changes in Caspase-3 apoptotic protein and activates cell apoptosis,while the Bax/Bcl-2 ratio showed no significant change.Claudin-2 protein likely modulates apoptosis through a caspase-3-dependent pathway independent of the Bax/Bcl-2 ratio.