ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2022
Activation of the NLRP3 inflammasome by RAC1 mediates a new mechanism in diabetic nephropathy.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 21 citations in OpenAlex.
- Mechanisms and Predisposing Conditions for Statin-Induced New-Onset Type 2 Diabetes Mellitus: A Paradox Relative to Their Pleiotropic Metabolic Effects.Endocrinology, diabetes & metabolism · 2026Review
- Neuroimmune Regulation by TRPM2 Channels.Cells · 2026Review
- Serum RAC1 as a potential biomarker in the early stages of diabetic kidney disease.Diabetology & metabolic syndrome · 2025Article
- Targeting RAC1 might be a potential therapeutic strategy for diabetic kidney disease: a Mendelian randomization study.International urology and nephrology · 2025Article
- Potential therapeutic effects of crocin.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Single-Cell RNA Sequencing Reveals RAC1 Involvement in Macrophages Efferocytosis in Diabetic Kidney Disease.Inflammation · 2024Article
- Single Nucleotide Polymorphisms of theBiomedicines · 2023Article
- Chronic kidney disease and NLRP3 inflammasome: Pathogenesis, development and targeted therapeutic strategies.Biochemistry and biophysics reports · 2023Review
- Role of Rho GTPases in inflammatory bowel disease.Cell death discovery · 2023Review
- Therapeutic potential of artemisinin and its derivatives in managing kidney diseases.Frontiers in pharmacology · 2023Review
- Natural products in attenuating renal inflammationFrontiers in immunology · 2023Review
- Rac1 as a Target to Treat Dysfunctions and Cancer of the Bladder.Biomedicines · 2022Review
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7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveInflammation is central to the development and progression of diabetic nephropathy (DN). Although the exact mechanisms of inflammation in the kidney have not been well elucidated, pyrin domain containing 3 (NLRP3) inflammasome activation is involved in the onset and progression of DN. Here, we investigated the underlying regulatory mechanisms of hyperglycaemia-induced NLRP3 inflammasome activation in the kidney.
methodsHEK293T cells received high glucose, and the cell proliferation and apoptosis were detected. Biochemical indicators in db/db mice were tested by kits, and the morphological changes in the kidney were observed using staining methods and transmission electron microscopy. The interaction of Ras-related C3 botulinum toxin substrate 1 (RAC1) and NLRP3 inflammasome in cells and in mice was assessed by co-immunoprecipitation (Co-IP) and immunofluorescence. Expression of all proteins was examined by western blotting and immunohistochemistry. In additional, the directly combination of RAC1 and NLRP3 was evaluated by GST Pulldown.
resultsHigh-glucose and hyperglycaemia conditions resulted in Ras-related C3 botulinum toxin substrate 1 (RAC1) and NLRP3 inflammasome interactions in cells and in mice. Additionally, RAC1 promoted NLRP3 inflammasome activation and then induced cell damage, and morphological and functional abnormalities in the kidney. We also observed that RAC1 activates the NLRP3 inflammasome by directly binding to NLRP3.
conclusionIn the present study, we confirmed that RAC1 binding to NLRP3 is sufficient to activate the NLRP3 inflammasome in the kidney and accelerate DN pathological processes. These results elucidate the upstream cellular and molecular mechanisms of NLRP3 inflammasome activation and provide new therapeutic strategies for the treatment of DN.
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