ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2014
Inhibition of hyperhomocysteinemia-induced inflammasome activation and glomerular sclerosis by NLRP3 gene deletion.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- C-reactive protein promotes diabetic kidney disease via Smad3-mediated NLRP3 inflammasome activation.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Podocyte-specific silencing of acid sphingomyelinase gene to abrogate hyperhomocysteinemia-induced NLRP3 inflammasome activation and glomerular inflammation.American journal of physiology. Renal physiology · 2024Article
- Resveratrol: A new approach to ameliorate hyperhomocysteinaemia-induced renal dysfunction.Experimental and therapeutic medicine · 2022Article
- Involvement of Inflammasome Components in Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Exosome Biogenesis and Lysosome Function Determine Podocyte Exosome Release and Glomerular Inflammatory Response during Hyperhomocysteinemia.The American journal of pathology · 2022Article
- Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway.Molecular medicine reports · 2021Article
- Controversies in Podocyte Loss: Death or Detachment?Frontiers in cell and developmental biology · 2021Review
- NLRP3 Inflammasome in Metabolic-Associated Kidney Diseases: An Update.Frontiers in immunology · 2021Review
- Inflammasome activation in podocytes: a new mechanism of glomerular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Review
- Control of lysosomal TRPML1 channel activity and exosome release by acid ceramidase in mouse podocytes.American journal of physiology. Cell physiology · 2019Article
- The role of inflammasomes in kidney disease.Nature reviews. Nephrology · 2019Review
- Rac1 GTPase Inhibition Blocked Podocyte Injury and Glomerular Sclerosis during Hyperhomocysteinemia via Suppression of Nucleotide-Binding Oligomerization Domain-Like Receptor Containing Pyrin Domain 3 Inflammasome Activation.Kidney & blood pressure research · 2019Article
- Inhibition of pannexin-1 channel activity by adiponectin in podocytes: Role of acid ceramidase activation.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Article
- NLRP3 inflammasome as a novel target for docosahexaenoic acid metabolites to abrogate glomerular injury.Journal of lipid research · 2017Article
- Trimethylamine-N-Oxide Instigates NLRP3 Inflammasome Activation and Endothelial Dysfunction.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2017Article
- High Prevalence of Hyperhomocysteinemia and Its Association with Target Organ Damage in Chinese Patients with Chronic Kidney Disease.Nutrients · 2016Article
- Toll-like receptor 4 mutation suppresses hyperhomocysteinemia-induced hypertension.American journal of physiology. Cell physiology · 2016Article
- Of Inflammasomes and Alarmins: IL-1β and IL-1α in Kidney Disease.Journal of the American Society of Nephrology : JASN · 2016Review
- Protective Action of Anandamide and Its COX-2 Metabolite against l-Homocysteine-Induced NLRP3 Inflammasome Activation and Injury in Podocytes.The Journal of pharmacology and experimental therapeutics · 2016Article
- Mesenchymal stem cell transplantation inhibited high salt-induced activation of the NLRP3 inflammasome in the renal medulla in Dahl S rats.American journal of physiology. Renal physiology · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND/
aimsHyperhomocysteinemia (hHcys) has been reported to initiate Nod-like receptor protein 3 (NLRP3) inflammasome formation and activation in podocytes, leading to glomerular dysfunction and sclerosis. However, it remains unknown whether Nlrp3 gene is critical for the formation and activation of inflammasomes in glomeruli of hHcys mice.
methodsPlasma homocysteine concentration was estimated utilizing HPLC, inflammasome formation and immunofluorescence expression from confocal microscopy, IL-1β production from ELISA.
resultsUninephrectomized Nlrp3 knockout (Nlrp3(-/-)) and wild type (Nlrp3(+/+)) and intra renal Nlrp3 shRNA-transfected wild type mice (Nlrp3 shRNA) were fed a folate free (FF) diet or normal chow (ND) for 4 weeks to produce hHcys. The plasma Hcys levels were significantly elevated in both Nlrp3(-/-) and Nlrp3(+/+) mice fed a FF diet compared to ND fed mice. The FF diet significantly increased the colocalization of Nlrp3 with apoptosis-associated speck-like protein (ASC) or caspase-1, caspase-1 activity and IL-1β production in glomeruli of Nlrp3(+/+), but not in Nlrp3(-/-) mice and local Nlrp3 shRNA transfected mice. Correspondingly, the glomerular damage index (GDI) and urinary protein excretion were significantly higher in Nlrp3(+/+) mice compared to ND fed mice. However, the hHcys-induced increase in GDI and proteinuria were significantly lower in Nlrp3(-/-) and local Nlrp3 shRNA transfected mice than in Nlrp3(+/+) mice. Immunocytochemical analysis showed that hHcys decreased expression of podocin and nephrin, but increased desmin expression in glomeruli of Nlrp3(+/+) mice compared to Nlrp3(-/-) mice.
conclusionNlrp3 gene is an essential component of Nlrp3 inflammasomes and that targeting Nlrp3 may be important therapeutic strategy to prevent inflammasome activation and thereby protect podocytes and glomeruli from hHcys-induced injury.
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