ArticleUrological research2012
Selective Rac1 inhibition protects renal tubular epithelial cells from oxalate-induced NADPH oxidase-mediated oxidative cell injury.
Article in Urological research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Probenecid protects against contrast-induced nephropathy through modulation of small Rho GTPases and Pannexin1 channels in Wistar rats.Clinical and experimental nephrology · 2025Article
- Network pharmacology and experimental validation to elucidate the pharmacological mechanisms of OATF against kidney stones.Frontiers in pharmacology · 2025Article
- Sigma-1 receptor exerts protective effects on ameliorating nephrolithiasis by modulating endoplasmic reticulum-mitochondrion association and inhibiting endoplasmic reticulum stress-induced apoptosis in renal tubular epithelial cells.Redox report : communications in free radical research · 2024Article
- Rac1 promotes kidney collecting duct repair by mechanically coupling cell morphology to mitotic entry.Science advances · 2024Article
- The Protective Role of Dietary Polyphenols in Urolithiasis: Insights into Antioxidant Effects and Mechanisms of Action.Nutrients · 2023Review
- Mineralocorticoid Receptor-Associated Mechanisms in Diabetic Kidney Disease and Clinical Significance of Mineralocorticoid Receptor Antagonists.American journal of nephrology · 2023Review
- Melatonin inhibits oxalate-induced endoplasmic reticulum stress and apoptosis in HK-2 cells by activating the AMPK pathway.Cell cycle (Georgetown, Tex.) · 2020Article
- Lysophosphatidic acid increases mesangial cell proliferation in models of diabetic nephropathy via Rac1/MAPK/KLF5 signaling.Experimental & molecular medicine · 2019Article
- The Protective Roles of Estrogen ReceptorOxidative medicine and cellular longevity · 2019Article
- The p21-activated kinase, PAK2, is important in the activation of numerous pancreatic acinar cell signaling cascades and in the onset of early pancreatitis events.Biochimica et biophysica acta · 2016Article
- Might E-cadherin promoter polymorphisms of rs16260 and rs5030625 associate with the risk of nephrolithiasis?SpringerPlus · 2016Article
- Involvement of renin-angiotensin-aldosterone system in calcium oxalate crystal induced activation of NADPH oxidase and renal cell injury.World journal of urology · 2016Article
- Association study of DGKH gene polymorphisms with calcium oxalate stone in Chinese population.Urolithiasis · 2014Article
- Reactive oxygen species, inflammation and calcium oxalate nephrolithiasis.Translational andrology and urology · 2014Article
- Article
- C-phycocyanin confers protection against oxalate-mediated oxidative stress and mitochondrial dysfunctions in MDCK cells.PloS one · 2014Article
- Reactive oxygen species as the molecular modulators of calcium oxalate kidney stone formation: evidence from clinical and experimental investigations.The Journal of urology · 2013Review
- Activation of Rac-1 and RhoA contributes to podocyte injury in chronic kidney disease.PloS one · 2013Article
- Is oxidative stress, a link between nephrolithiasis and obesity, hypertension, diabetes, chronic kidney disease, metabolic syndrome?Urological research · 2012Review
- Effects of different concentrations of artemisinin and artemisinin-iron combination treatment on Madin Darby Canine Kidney (MDCK) cells.Interdisciplinary toxicology · 2012Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Oxalate-induced oxidative cell injury is one of the major mechanisms implicated in calcium oxalate nucleation, aggregation and growth of kidney stones. We previously demonstrated that oxalate-induced NADPH oxidase-derived free radicals play a significant role in renal injury. Since NADPH oxidase activation requires several regulatory proteins, the primary goal of this study was to characterize the role of Rac GTPase in oxalate-induced NADPH oxidase-mediated oxidative injury in renal epithelial cells. Our results show that oxalate significantly increased membrane translocation of Rac1 and NADPH oxidase activity of renal epithelial cells in a time-dependent manner. We found that NSC23766, a selective inhibitor of Rac1, blocked oxalate-induced membrane translocation of Rac1 and NADPH oxidase activity. In the absence of Rac1 inhibitor, oxalate exposure significantly increased hydrogen peroxide formation and LDH release in renal epithelial cells. In contrast, Rac1 inhibitor pretreatment, significantly decreased oxalate-induced hydrogen peroxide production and LDH release. Furthermore, PKC α and δ inhibitor, oxalate exposure did not increase Rac1 protein translocation, suggesting that PKC resides upstream from Rac1 in the pathway that regulates NADPH oxidase. In conclusion, our data demonstrate for the first time that Rac1-dependent activation of NADPH oxidase might be a crucial mechanism responsible for oxalate-induced oxidative renal cell injury. These findings suggest that Rac1 signaling plays a key role in oxalate-induced renal injury, and may serve as a potential therapeutic target to prevent calcium oxalate crystal deposition in stone formers and reduce recurrence.
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