ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2019
Podocyte NLRP3 Inflammasome Activation and Formation by Adipokine Visfatin.
Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Downregulation of CXCL16/ADAM10 axis by Simvastatin attenuates tacrolimus-induced tubulointerstitial fibrosis.Scientific reports · 2026Article
- The lipid-podocyte axis: emerging clues in membranous nephropathy pathogenesis.Frontiers in medicine · 2026Review
- NLRP3 Inflammasome as Potential Predictor of Non-Responsiveness to Immunosuppressive Treatment in Lupus Nephritis.International journal of molecular sciences · 2025Article
- Understanding the Role of Adipokines in Cardiometabolic Dysfunction: A Review of Current Knowledge.Biomolecules · 2025Review
- Acid Sphingomyelinase and Ceramide Signaling Pathway Mediates Nicotine-Induced NLRP3 Inflammasome Activation and Podocyte Injury.Biomedicines · 2025Article
- High mobility group box 1 (HMGB1) mediates nicotine-induced podocyte injury.Frontiers in pharmacology · 2024Article
- Article
- Regulation of NLRP3 Inflammasome Activation and Inflammatory Exosome Release in Podocytes by Acid Sphingomyelinase During Obesity.Inflammation · 2023Article
- ADAM metallopeptidase domain 10 knockdown enables podocytes to resist high glucose stimulation by inhibiting pyroptosis via MAPK pathway.Experimental and therapeutic medicine · 2023Article
- No NLRP3 inflammasome activity in kidney epithelial cells, not even when the NLRP3-A350V Muckle-Wells variant is expressed in podocytes of diabetic mice.Frontiers in immunology · 2023Article
- Renoprotection by Inhibiting Connexin 43 Expression in a Mouse Model of Obesity-Related Renal Injury.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- Extracellular nicotinamide phosphoribosyltransferase: role in disease pathophysiology and as a biomarker.Frontiers in immunology · 2023Review
- Targeting Pyroptosis: New Insights into the Treatment of Diabetic Microvascular Complications.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Review
- The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.Frontiers in cell and developmental biology · 2020Review
- Role of Inflammasomes in Kidney Diseases via Both Canonical and Non-canonical Pathways.Frontiers in cell and developmental biology · 2020Review
- Article
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Authors and funding
6 authors.
Funding
Abstract
BACKGROUND/
aimsNLRP3 inflammasome activation has been reported to be an early mechanism responsible for glomerular inflammation and injury in obese mice. However, the precise mechanism of obesity-induced NLRP3 inflammasome activation remains unknown. The present study explored whether adipokine visfatin mediates obesity-induced NLRP3 inflammasome activation and consequent podocyte injury.
methodsInflammasome formation and immunofluorescence expressions were quantified by confocal microscopy. Caspase-activity, IL-1β production and VEGF concentrations were measured by ELISA.
resultsConfocal microscopic analysis showed that visfatin treatment increased the colocalization of Nlrp3 with Asc or Nlrp3 with caspase-1 in podocytes indicating the formation of NLRP3 inflammasomes. This visfatin-induced NLRP3 inflammasome formation was abolished by pretreatment of podocytes with Asc siRNA. Correspondingly, visfatin treatment significantly increased the caspase-1 activity and IL-1β production in podocytes, which was significantly attenuated by Asc siRNA transfection. Further RT-PCR and confocal microscopic analysis demonstrated that visfatin treatment significantly decreased the podocin expression (podocyte damage). Podocytes pretreatment with Asc siRNA or caspase-1 inhibitor, WEHD attenuated this visfatin-induced podocin reduction. Furthermore, Asc siRNA transfection was found to preserve podocyte morphology by maintaining the distinct arrangement of F-actin fibers normally lost in response to visfatin. It also prevented podocyte dysfunction by restoring visfatin-induced suppression of VEGF production and secretion.
conclusionVisfatin induces NLRP3 inflammasome activation in podocytes and thereby resulting in podocyte injury.
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