ArticleUrolithiasis2026
EP3 receptor mediates calcium oxalate kidney stone formation via Ca²⁺/AKT and necroinflammation.
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
Kidney stone disease is a prevalent urological condition with rising incidence and high recurrence rates, yet effective pharmacological interventions remain lacking [1] Prostaglandin E₂ (PGE₂) and its receptor EP3 have been implicated in inflammatory kidney injury [1-3], but their role in nephrolithiasis is unclear. This study investigates the role and mechanism of EP3 in calcium oxalate (CaOx) stone formation using in vitro and in vivo models. EP3 expression was significantly upregulated in CaOx-stimulated human renal tubular epithelial cells (HK-2) and in kidney tissues of glyoxylate-induced nephrolithiasis mice. Treatment with the EP3 antagonist DG041 in vitro reduced crystal adhesion, decreased HMGB1 release, and suppressed IL-6 and TNF-α expression. Mechanistically, EP3 antagonism inhibited aberrant intracellular Ca
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