ArticleThe Journal of biological chemistry2014
Nod-like receptor protein 3 (NLRP3) inflammasome activation and podocyte injury via thioredoxin-interacting protein (TXNIP) during hyperhomocysteinemia.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 145 citations in OpenAlex.
- 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
- Targeting NLRP3 inflammasome to mitigate chemotherapy-induced cardiotoxicity: advances in selective inhibitors and natural modulators.Molecular biology reports · 2026Review
- The PVAT-MAMs Axis in Atherosclerosis: A Hypothesis-Driven Cross-Scale Conceptual Framework.International journal of molecular sciences · 2026Review
- The selenium-enrichedFrontiers in microbiology · 2026Article
- Acid ceramidase as a novel target for adiponectin receptor agonist to abrogate podocyte NLRP3 inflammasome activation and glomerular inflammation during obesity.The Journal of pharmacology and experimental therapeutics · 2025Article
- Mechanisms of NLRP3 inflammasome in chronic kidney disease and the effects of traditional Chinese medicines.Renal failure · 2025Review
- Uncovering Hyperhomocysteinemia: Global Risk Patterns and Molecular Disruption in Brain and Vascular Health.Journal of neurochemistry · 2025Review
- The NOX2-ROS-NLRP3 inflammasome axis in traumatic brain injury.Journal of neuroinflammation · 2025Article
- MicroRNA-204-5p Attenuates Oxidative Stress, Apoptosis and Inflammation by Targeting TXNIP in Diabetic Cataract.Biochemical genetics · 2025Article
- Ginsenoside Rg5 modulates the TLR4 and BCL-2 pathways by inhibiting NOX1, thereby alleviating inflammation, apoptosis and pyroptosis in hyperuricemia nephropathy.Journal of ginseng research · 2025Article
- Mitigation of nicotine-induced podocyte injury through inhibition of thioredoxin interacting protein.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Correlation of Neuroinflammation and Therapeutic Targets in Perioperative Neurocognitive Disorders.Current pharmaceutical biotechnology · 2025Review
- Research Progress on Podocyte Pyroptosis in Diabetic Nephropathy.Current medicinal chemistry · 2025Review
- Advances in kidney disease: pathogenesis and therapeutic targets.Frontiers in medicine · 2025Review
- Endoplasmic Reticulum Stress Induces ROS Production and Activates NLRP3 Inflammasome Via the PERK-CHOP Signaling Pathway in Dry Eye Disease.Investigative ophthalmology & visual science · 2024Article
- Epigallocatechin-3-Gallate Ameliorates Diabetic Kidney Disease by Inhibiting the TXNIP/NLRP3/IL-1β Signaling Pathway.Food science & nutrition · 2024Article
- Podocyte-specific silencing of acid sphingomyelinase gene to abrogate hyperhomocysteinemia-induced NLRP3 inflammasome activation and glomerular inflammation.American journal of physiology. Renal physiology · 2024Article
- High Starch Induces Hematological Variations, Metabolic Changes, Oxidative Stress, Inflammatory Responses, and Histopathological Lesions in Largemouth Bass (Metabolites · 2024Article
- Co-Treatment with Phlorotannin and Extracellular Vesicles fromAntioxidants (Basel, Switzerland) · 2024Article
- Narirutin Attenuates Cerebral Ischemia-Reperfusion Injury by Suppressing the TXNIP/NLRP3 Pathway.Neurochemical research · 2024Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
NADPH oxidase-derived reactive oxygen species (ROS) have been reported to activate NLRP3 inflammasomes resulting in podocyte and glomerular injury during hyperhomocysteinemia (hHcys). However, the mechanism by which the inflammasome senses ROS is still unknown in podocytes upon hHcys stimulation. The current study explored whether thioredoxin-interacting protein (TXNIP), an endogenous inhibitor of the antioxidant thioredoxin and ROS sensor, mediates hHcys-induced NLRP3 inflammasome activation and consequent glomerular injury. In cultured podocytes, size exclusion chromatography and confocal microscopy showed that inhibition of TXNIP by siRNA or verapamil prevented Hcys-induced TXNIP protein recruitment to form NLRP3 inflammasomes and abolished Hcys-induced increases in caspase-1 activity and IL-1β production. TXNIP inhibition protected podocytes from injury as shown by normal expression levels of podocyte markers, podocin and desmin. In vivo, adult C57BL/6J male mice were fed a folate-free diet for 4 weeks to induce hHcys, and TXNIP was inhibited by verapamil (1 mg/ml in drinking water) or by local microbubble-ultrasound TXNIP shRNA transfection. Evidenced by immunofluorescence and co-immunoprecipitation studies, glomerular inflammasome formation and TXNIP binding to NLRP3 were markedly increased in mice with hHcys but not in TXNIP shRNA-transfected mice or those receiving verapamil. Furthermore, TXNIP inhibition significantly reduced caspase-1 activity and IL-1β production in glomeruli of mice with hHcys. Correspondingly, TXNIP shRNA transfection and verapamil attenuated hHcys-induced proteinuria, albuminuria, glomerular damage, and podocyte injury. In conclusion, our results demonstrate that TXNIP binding to NLRP3 is a key signaling mechanism necessary for hHcys-induced NLRP3 inflammasome formation and activation and subsequent glomerular injury.
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