ArticleJournal of diabetes research2015
NADPH oxidase-induced NALP3 inflammasome activation is driven by thioredoxin-interacting protein which contributes to podocyte injury in hyperglycemia.
Article in Journal of diabetes research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 82 citations in OpenAlex.
- Mitigation of nicotine-induced podocyte injury through inhibition of thioredoxin interacting protein.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Beyond Redox Regulation: Novel Roles of TXNIP in the Pathogenesis and Therapeutic Targeting of Kidney Disease.The American journal of pathology · 2025Review
- Xanthohumol attenuates TXNIP-mediated renal tubular injury in vitro and in vivo diabetic models.Journal of natural medicines · 2025Article
- Research Progress on Podocyte Pyroptosis in Diabetic Nephropathy.Current medicinal chemistry · 2025Review
- Targeting the NLRP3 inflammasome in kidney disease: molecular mechanisms, pathogenic roles, and emerging small-molecule therapeutics.Frontiers in immunology · 2025Review
- Mechanisms and Targeted Therapeutic Strategies in Sepsis-Induced Myocardial Dysfunction: The Role of NLRP3 Inflammasome-Mediated Inflammation.Journal of inflammation research · 2025Review
- Anti-Inflammatory Effects of Extracellular Vesicles fromInternational journal of molecular sciences · 2024Article
- Role of the Innate Immune Response in Glomerular Disease Pathogenesis: Focus on Podocytes.Cells · 2024Review
- Co-Treatment with Phlorotannin and Extracellular Vesicles fromAntioxidants (Basel, Switzerland) · 2024Article
- The role of innate immunity in diabetic nephropathy and their therapeutic consequences.Journal of pharmaceutical analysis · 2024Review
- Research progress on multiple cell death pathways of podocytes in diabetic kidney disease.Molecular medicine (Cambridge, Mass.) · 2023Review
- TXNIP: A key protein in the cellular stress response pathway and a potential therapeutic target.Experimental & molecular medicine · 2023Review
- Lysophosphatidic Acid Induces Podocyte Pyroptosis in Diabetic Nephropathy by an Increase of Egr1 Expression via Downregulation of EzH2.International journal of molecular sciences · 2023Article
- The Role of Histone Modifications in the Pathogenesis of Diabetic Kidney Disease.International journal of molecular sciences · 2023Review
- Natural products in attenuating renal inflammationFrontiers in immunology · 2023Review
- Novel insights into NOD-like receptors in renal diseases.Acta pharmacologica Sinica · 2022Review
- Targeting the NLRP3 inflammasome in cardiovascular diseases.Pharmacology & therapeutics · 2022Review
- Neuroinflammation and COVID-19 Ischemic Stroke Recovery-Evolving Evidence for the Mediating Roles of the ACE2/Angiotensin-(1-7)/Mas Receptor Axis and NLRP3 Inflammasome.International journal of molecular sciences · 2022Review
- Involvement of Inflammasome Components in Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Epigenetics and endoplasmic reticulum in podocytopathy during diabetic nephropathy progression.Frontiers in immunology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is one of the major causes of end-stage renal disease, and previously we demonstrated that NALP3 inflammasome was involved in the pathogenesis of DN. Here we investigated the mechanisms of NALP3 inflammasome activation in podocyte injury during DN. We found that, besides the activation of NALP3 inflammasome and upregulated thioredoxin-interacting protein (TXNIP), the glomerular expression of gp91 (phox) , a subunit of NADPH oxidase, was enhanced in DN mice simultaneously. Inhibiting NADPH oxidase abrogated NALP3 inflammasome activation, and IL-1β production and eventually protected podocytes from high glucose- (HG-) induced injury. TXNIP, an inhibitor of thioredoxin, acts as a suppressor for antioxidant defense system. Our observation indicated that in HG-exposed podocytes genetic deletion of TXNIP by shRNA reversed gp91 (phox) overexpression and alleviated the injury of podocyte. Collectively, our findings proposed that HG-induced NADPH oxidase activation was driven by TXNIP which subsequently triggered NALP3 inflammasome activation in podocytes and ultimately led to podocyte injury, and blocking TXNIP/NADPH oxidase signaling may be a promising treatment for DN.
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