ArticleBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2025
Mitigation of nicotine-induced podocyte injury through inhibition of thioredoxin interacting protein.
Article in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Sacubitril/valsartan attenuates renal injury caused by cecal ligation and puncture via TLR4/NFκB/NLRP3 inhibition and reduced oxidative stress and apoptosis in rats.Scientific reports · 2026Article
- Nrf2 promotes NLRP3 inflammasome assembly and activation by Klf9-TXNIP axis.Cell death discovery · 2026Article
- Colchicine attenuates kidney injury by modulating the NLRP3 inflammasome pathway.Molecular medicine (Cambridge, Mass.) · 2026Article
- Downregulation of CXCL16/ADAM10 axis by Simvastatin attenuates tacrolimus-induced tubulointerstitial fibrosis.Scientific reports · 2026Article
- Regulated cell death: a multidimensional regulatory network in the pathogenesis of renal fibrosis.Apoptosis : an international journal on programmed cell death · 2026Review
- The selenium-enrichedFrontiers in microbiology · 2026Article
- A novel redox signalling axis mediates nicotine-induced podocyte injury.Frontiers in pharmacology · 2026Article
- Nicotinism vs. Glomerulopathies-Smoking as a Risk Factor for Primary Glomerulopathies.Antioxidants (Basel, Switzerland) · 2025Review
- Overlapping risk factors and pathogenic mechanisms in lung cancer and cardiovascular disease.Discover oncology · 2025Review
- Comparative effectiveness and pharmacological fingerprints of indobufen versus rivaroxaban in patients with chronic kidney disease: a single-center, real-world study.Frontiers in pharmacology · 2025Article
- Licorice in nephropathy treatment: phytochemical compositions and pharmacological mechanisms.Frontiers in pharmacology · 2025Review
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Authors and funding
4 authors.
Funding
Abstract
Nicotine has been reported to initiate NLRP3 inflammasome formation and activation in different pathological conditions. The current study assessed whether thioredoxin-interacting protein (TXNIP) mediates nicotine-induced NLRP3 inflammasome activation and consequent podocyte injury. Co-immunoprecipitation analysis demonstrated that nicotine-induced TXNIP/NLRP3 interaction in podocytes relative to control groups. However, pre-treatment with TXNIP inhibitors, verapamil (Vera) or SRI-37330 (SRI) attenuates nicotine-induced TXNIP/NLRP3 interaction. Confocal microscopic analysis showed that nicotine treatment significantly increased the colocalization of Nlrp3 with Asc, Nlrp3 with caspase-1 and Nlrp3 with TXNIP in podocytes compared to control cells. Pretreatment with TXNIP inhibitor Vera or SRI abolished nicotine-induced Nlrp3/Asc, Nlrp3/caspase-1 or Nlrp3/TXNIP colocalization. Correspondingly, nicotine treatment significantly increased the caspase-1 activity and IL-1β production compared to control cells. However, prior treatment with TXNIP inhibiting Vera or SRI significantly attenuated the nicotine-induced caspase-1 activity and IL-1β production. Further immunofluorescence analysis showed that nicotine treatment significantly decreased podocin and nephrin expression compared to control cells. However, pretreatment with TXNIP inhibiting Vera or SRI attenuated the nicotine-induced podocin and nephrin reduction. In addition, confocal, flow cytometry and biochemical analysis showed that nicotine treatment significantly increased desmin expression, apoptosis and cell permeability compared to control cells. However, prior treatment with TXNIP inhibiting Vera or SRI significantly attenuated the nicotine-induced desmin expression, apoptosis and cell permeability. Taken together, our results demonstrate that TXNIP/NLRP3 interaction constitutes a potentially key signalling mechanism driving nicotine-induced NLRP3 inflammasome formation, activation and subsequent podocyte damage.
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