ArticleFree radical biology & medicine2014
Contribution of endogenously produced reactive oxygen species to the activation of podocyte NLRP3 inflammasomes in hyperhomocysteinemia.
Article in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 83 citations in OpenAlex.
- Advances and perspectives of functional nanomaterials in scavenging reactive oxygen species for acute kidney injury.Bioactive materials · 2026Review
- Natural Plant-Derived Compounds Targeting Oxidative Stress and Inflammation in NAFLD-Mechanisms and Repositioning Potential.Current issues in molecular biology · 2026Review
- Podocyte-specific acid sphingomyelinase overexpression promotes gasdermin D dependent pyroptosis by impairing autophagic flux during obesity.Frontiers in physiology · 2026Article
- Integrated mechanisms linking sodium-potassium imbalance to salt-sensitive hypertension.Physiological reports · 2025Review
- 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
- Review
- Mitigation of nicotine-induced podocyte injury through inhibition of thioredoxin interacting protein.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Sphingolipid signaling in kidney diseases.American journal of physiology. Renal physiology · 2025Review
- Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025Review
- Podocyte-specific silencing of acid sphingomyelinase gene to abrogate hyperhomocysteinemia-induced NLRP3 inflammasome activation and glomerular inflammation.American journal of physiology. Renal physiology · 2024Article
- Energy substrate metabolism and oxidative stress in metabolic cardiomyopathy.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Bee Venom Induces Acute Inflammation through a HToxins · 2022Article
- Mitochondrial Oxidative Stress and Cell Death in Podocytopathies.Biomolecules · 2022Review
- Hepatitis B virus X mediates podocyte pyroptosis by regulating the ROS/NLRP3 signaling pathway in hepatitis B virus-associated glomerulonephritis.Iranian journal of basic medical sciences · 2022Article
- Sappanone a prevents diabetic kidney disease by inhibiting kidney inflammation and fibrosisFrontiers in pharmacology · 2022Article
- Exosome Biogenesis and Lysosome Function Determine Podocyte Exosome Release and Glomerular Inflammatory Response during Hyperhomocysteinemia.The American journal of pathology · 2022Article
- Inflammation and oxidative stress in salt sensitive hypertension; The role of the NLRP3 inflammasome.Frontiers in physiology · 2022Review
- Salt Sensitivity of Blood Pressure in Blacks and Women: A Role of Inflammation, Oxidative Stress, and Epithelial NaAntioxidants & redox signaling · 2021Review
- Regulation of TRPML1 channel activity and inflammatory exosome release by endogenously produced reactive oxygen species in mouse podocytes.Redox biology · 2021Article
- Contribution of podocyte inflammatory exosome release to glomerular inflammation and sclerosis during hyperhomocysteinemia.Biochimica et biophysica acta. Molecular basis of disease · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Hyperhomocysteinemia (hHcys) is an important pathogenic factor contributing to the progression of end-stage renal disease. Recent studies have demonstrated the implication of nicotinamide adenine dinucleotide phosphate oxidase-mediated NLRP3 inflammasome activation in the development of podocyte injury and glomerular sclerosis during hHcys. However, it remains unknown which reactive oxygen species (ROS) are responsible for this activation of NLRP3 inflammasomes and how such action of ROS is controlled. This study tested the contribution of common endogenous ROS including superoxide (O2(-)), hydrogen peroxide (H2O2), peroxynitrite (ONOO(-)), and hydroxyl radical (OH) to the activation of NLRP3 inflammasomes in mouse podocytes and glomeruli. In vitro, confocal microscopy and size-exclusion chromatography demonstrated that dismutation of O2(-) by 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (Tempol) and decomposition of H2O2 by catalase prevented Hcys-induced aggregation of NLRP3 inflammasome proteins and inhibited Hcys-induced caspase-1 activation and IL-1β production in mouse podocytes. However, scavenging of ONOO(-) or OH had no significant effect on either Hcys-induced NLRP3 inflammasome formation or activation. In vivo, scavenging of O2(-) by Tempol and removal of H2O2 by catalase substantially inhibited NLRP3 inflammasome formation and activation in glomeruli of hHcys mice as shown by reduced colocalization of NLRP3 with ASC or caspase-1 and inhibition of caspase-1 activation and IL-1β production. Furthermore, Tempol and catalase significantly attenuated hHcys-induced glomerular injury. In conclusion, endogenously produced O2(-) and H2O2 primarily contribute to NLRP3 inflammasome formation and activation in mouse glomeruli resulting in glomerular injury or consequent sclerosis during hHcys.
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