ArticleUrolithiasis2026
Mechanism of claudin-2 in RTECs apoptosis after renal obstruction.
Article in Urolithiasis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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