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Mechanism of claudin-2 in RTECs apoptosis after renal obstruction

Dongsheng Zhao1, Guijiang Tang1, Guoqian Hu1

  • 1Department of Urology, The Third Hospital Central South University, 138 Tongzipo Road, Yuelu District, Hexi District, Changsha, Hunan, China.

Urolithiasis
|July 2, 2026
PubMed

Insights

Claudin-2 expression decreases in acute kidney injury (AKI), promoting renal tubular cell apoptosis via the caspase-3 pathway. Restoring Claudin-2 levels protects kidney cells from injury.

Area of Science:

  • Nephrology
  • Cell Biology
  • Molecular Medicine

Background:

  • Acute kidney injury (AKI) is a critical condition often caused by renal obstruction, leading to tubular epithelial cell damage.
  • Understanding the molecular mechanisms of AKI, particularly the role of specific proteins in cell apoptosis, is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of Claudin-2 in renal tubular epithelial cell apoptosis during ischemia-induced AKI.
  • To determine the specific pathway through which Claudin-2 influences cell death in AKI.

Main Methods:

  • Utilized a mouse model of unilateral ureteral obstruction (UUO) and oxygen-glucose deprivation (OGD) in HK-2 cells to mimic ischemic AKI.
  • Assessed protein expression levels of Claudin-2, Bax, Bcl-2, and Caspase-3.
  • Employed lentivirus transfection to upregulate Claudin-2 expression in OGD-treated cells.

Main Results:

  • Claudin-2 expression was significantly decreased in both UUO mice and OGD-treated HK-2 cells.
  • Decreased Claudin-2 correlated with increased Bax and Caspase-3, and decreased Bcl-2 expression.
  • Upregulating Claudin-2 in HK-2 cells reduced apoptosis and cell death, and decreased Caspase-3 levels, independent of the Bax/Bcl-2 ratio.

Conclusions:

  • Claudin-2 expression is downregulated in acute obstructive kidney injury.
  • Reduced Claudin-2 contributes to renal tubular cell apoptosis through a caspase-3-dependent pathway.
  • Claudin-2 may serve as a potential therapeutic target for mitigating AKI-associated apoptosis.
Keywords:
Acute kidney injuryApoptosis of cellsClaudin-2RTECsRenal ischemiaRenal obstruction

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