ArticleLupus2013
NADPH oxidase and nitric oxide synthase-dependent superoxide production is increased in proliferative lupus nephritis.
Article in Lupus, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Immune imbalance in Lupus Nephritis: The intersection of T-Cell and ferroptosis.Frontiers in immunology · 2024Review
- The Role of the Oxidative State and Innate Immunity Mediated by TLR7 and TLR9 in Lupus Nephritis.International journal of molecular sciences · 2023Review
- Biomarkers of Oxidative Stress in Systemic Lupus Erythematosus Patients with Active Nephritis.Antioxidants (Basel, Switzerland) · 2023Article
- A Rheostat of Ceramide and Sphingosine-1-Phosphate as a Determinant of Oxidative Stress-Mediated Kidney Injury.International journal of molecular sciences · 2022Review
- Iron Metabolism: An Under Investigated Driver of Renal Pathology in Lupus Nephritis.Frontiers in medicine · 2021Review
- Lupus serum induces inflammatory interaction with neutrophils in human glomerular endothelial cells.Lupus science & medicine · 2020Article
- ASSOCIATIONS BETWEEN ACCELERATED ATHEROSCLEROSIS, OXIDIZED LDL IMMUNE COMPLEXES, AND IN VITRO ENDOTHELIAL DYSFUNCTION IN SYSTEMIC LUPUS ERYTHEMATOSUS.Transactions of the American Clinical and Climatological Association · 2020Article
- Lipopolysaccharide induces inducible nitric oxide synthase-dependent podocyte dysfunction via a hypoxia-inducible factor 1α and cell division control protein 42 and Ras-related C3 botulinum toxin substrate 1 pathway.Free radical biology & medicine · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveLupus nephritis (LN) is an immune complex-mediated glomerulonephritis. Proliferative LN (PLN, ISN/RPS classes III and IV)) often leads to renal injury or failure despite traditional induction and maintenance therapy. Successful targeted therapeutic development requires insight into mediators of inflammation in PLN. Superoxide (SO) and its metabolites are mediators of the innate immune response through their ability to mediate reduction-oxidation signaling. Endothelial nitric oxide synthase (eNOS) modulates inflammatory responses in endothelial cells. We hypothesized that markers of SO production would be increased in active PLN and that SO production would be dependent on the activity of select enzymes in the renal cortex.
methodsPatients with systemic lupus erythematosus were enrolled at the time of renal biopsy for active LN of all classes. Serum collected at baseline was analyzed by HPLC with electrochemical detection for markers of SO production (durable modifications of serum protein Tyr ultimately requiring SO as a substrate). Renal cortex from MRL/MpJ-FAS(lpr) (MRL/lpr) mice with and without functional eNOS was analyzed during active disease for superoxide (SO) production with and without inhibitors of SO-producing enzymes.
resultsSerum protein modifications indicative of total SO production were significantly higher in patients with PLN. These markers were increased in association with more active, inflammatory PLN. Mice lacking functional eNOS had 80% higher levels of renal cortical SO during active disease, and inhibitors of nitric oxide synthase and NADPH oxidase reduced these levels by 60% and 77%, respectively.
conclusionThese studies demonstrate that SO production is unique to active PLN in a NOS and NADPH oxidase-dependent fashion. These findings suggest the emulating or augmenting eNOS activity or inhibiting NADPH oxidase SO production may be targets of therapy in patients with PLN. The markers of SO production used in this study could rationally be used to select SO-modulating therapies and serve as pharmacodynamic indicators for dose titration.
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Registered trials
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