Skip to content

EP3 receptor mediates calcium oxalate kidney stone formation via Ca²⁺/AKT and necroinflammation

Aug 2026 · Urolithiasis · Vol 54 · 0 citations · 29 references
Medicine

TL;DR

It is demonstrated that the EP3 receptor mediates calcium oxalate kidney stone formation through the Ca2⁺/AKT signaling pathway and necroinflammation through the Ca2⁺/AKT signaling axis.

View source

Similar papers

Open access Oct 2026

Acacetin alleviates pyroptosis, inflammatory response, and oxidative stress in renal tubular epithelial cells caused by kidney stone via targeting GPR35.

Nephrolithiasis, particularly calcium oxalate (CaOx) stones, remains a global health burden with limited pharmacological options for recurrence prevention. In this study, we investigated the therapeutic mechanism of acacetin (ACA) using both in vitro (COM-stimulated HK-2 cells) and in vivo (glyoxylate-induced mice) mod...

Lei Jiang, Qing-Yan Xia, Zhong-Wen Hong et al. · 0 citations
Sep 2026

β-carotene attenuates calcium oxalate crystal-induced renal injury through suppression of NF-κB-mediated inflammation

Findings indicate that β-carotene ameliorates CaOx crystal-induced renal injury and inflammation, at least in part through suppression of NF-κB signaling, and may offer a potential basis for the development of novel preventive and therapeutic approaches for kidney stone disease.

Ming-Qin Su, Yu-Xiang Guan, Hong-Quan Wei et al. · 0 citations
Open access Oct 2026

Interleukin-37 does not confer protection against stone formation or kidney injury at the peak of disease in a murine calcium oxalate model

Calcium oxalate (CaOx) stones are the most prevalent form of nephrolithiasis in adults. While murine models of CaOx stone disease are established, many lack translational features for therapeutic evaluation, including in vivo assessment of kidney function and molecular profiling of renal inflammation. We refined the gl...

N. Bhatt, Theresa T. Nguyen, I. Rudloff et al. · 0 citations
Sep 2026

Complanatuside Ameliorates Renal Injury and Fibrosis in Chronic Kidney Disease by Inhibiting Tubular Cell Apoptosis via Activation of KLK1/BDKRB2.

It is found that CPT binds to KLK1, activates its expression, reduces PTEC apoptosis, and thereby attenuates renal fibrosis, and reveals that CPT binds to KLK1, promotes BDKRB2 expression, thereby reducing PTEC apoptosis and improving renal fibrosis.

Jing Gao, Rui-Zhi Tan, K. Deng et al. · 0 citations
Open access Oct 2026

Group IVA Cytosolic Phospholipase A2 (cPLA2α): Pharmacological Inhibition Attenuates Kidney Inflammation and Fibrosis

Chronic kidney disease (CKD) is a significant global health burden and a leading cause of death in the United States. Chronic inflammation contributes to fibrosis and CKD progression. Here, we present evidence that a key pro-inflammatory group IVA phospholipase A2 enzyme (cPLA2α) is critical to the development of kidne...

Berit Johansen, Said Movahedinaini, L. Selvik et al. · 0 citations

We use cookies to run the site and, with your consent, for analytics and to show ads. See our Cookie Policy.