ArticleJournal of the American Society of Nephrology : JASN2015
Extracellular Superoxide Dismutase Protects against Proteinuric Kidney Disease.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Superoxide Dismutase Administration: A Review of Proposed Human Uses.Molecules (Basel, Switzerland) · 2021Pooled it
- The gut-brain axis and inflammatory mediators in suicide and mental disorders with high suicide rates: a review of current evidence.Dialogues in clinical neuroscience · 2026Review
- Anti-ANGPTL3 antibody and IL-22 fusion protein mitigate nephrotic syndrome via mitochondrial protection, anti-apoptosis, and autophagy suppression.Antibody therapeutics · 2026Article
- Extracellular Superoxide Dismutase in Acute Respiratory Distress Syndrome: Pathogenic Mechanisms and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2026Review
- Vascular Calcification in Chronic Kidney Disease and Hemodialysis: Pathophysiological Mechanisms and Emerging Biomarkers.Medicina (Kaunas, Lithuania) · 2025Review
- Deacetylation of SOD3 by sirtuins restores furin cleavage.Redox biochemistry and chemistry · 2025Article
- From Wild Vegetable to Renal Protector: The Therapeutic Potential ofFood science & nutrition · 2025Article
- Unveiling mechanisms underlying kidney function changes during sex hormone therapy.The Journal of clinical investigation · 2025Observational
- Non-Thyroidal Illness in Chronic Renal Failure: Triiodothyronine Levels and Modulation of Extra-Cellular Superoxide Dismutase (ec-SOD).Antioxidants (Basel, Switzerland) · 2024Article
- Alleviation of ischemia-reperfusion induced renal injury by chemically modifiedMolecular therapy. Nucleic acids · 2023Article
- Therapeutic potential of artemisinin and its derivatives in managing kidney diseases.Frontiers in pharmacology · 2023Review
- Moderate hyperuricaemia ameliorated kidney damage in a low-renin model of experimental renal insufficiency.Basic & clinical pharmacology & toxicology · 2023Article
- Nonsteroidal Mineralocorticoid Receptor Antagonism by Finerenone-Translational Aspects and Clinical Perspectives across Multiple Organ Systems.International journal of molecular sciences · 2022Review
- Bisdemethoxycurcumin Attenuated Renal Injury via Activation of Keap1/Nrf2 Pathway in High-Fat Diet-Fed Mice.International journal of molecular sciences · 2022Article
- Mechanisms of podocyte injury and implications for diabetic nephropathy.Clinical science (London, England : 1979) · 2022Article
- Superoxide dismutase 3 prevents early stage diabetic retinopathy in streptozotocin-induced diabetic rat model.PloS one · 2022Article
- Renoprotective potentials of small molecule natural products targeting mitochondrial dysfunction.Frontiers in pharmacology · 2022Review
- Morphometric Effects of HO-1 Deficiency and Overexpression in Rat Glomeruli and Podocytes.Journal of clinical & anatomic pathology (JCAP) · 2021Article
- Protective effect of alamandine on doxorubicin‑induced nephrotoxicity in rats.BMC pharmacology & toxicology · 2021Article
- Association among extracellular superoxide dismutase genotype, plasma concentration, and comorbidity in the very old and centenarians.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Extracellular superoxide dismutase (EC-SOD), also known as SOD3, is an antioxidant expressed at high levels in normal adult kidneys. Because oxidative stress contributes to a variety of kidney injuries, we hypothesized that EC-SOD may be protective in CKD progression. To study this hypothesis, we used a murine model of ADR nephropathy characterized by albuminuria and renal dysfunction. We found that levels of EC-SOD diminished throughout the course of disease progression and were associated with increased levels of NADPH oxidase and oxidative stress markers. EC-SOD null mice were sensitized to ADR injury, as evidenced by increases in albuminuria, serum creatinine, histologic damage, and oxidative stress. The absence of EC-SOD led to increased levels of NADPH oxidase and an increase in β-catenin signaling, which has been shown to be pathologic in a variety of kidney injuries. Exposure of EC-SOD null mice to either chronic angiotensin II infusion or to daily albumin injections also caused increased proteinuria. In contrast, EC-SOD null mice subjected to nonproteinuric CKD induced by unilateral ureteral obstruction exhibited no differences compared with wild-type mice. Finally, we also found a decrease in EC-SOD in human CKD biopsy samples, similar to our findings in mice. Therefore, we conclude that EC-SOD is protective in CKDs characterized by proteinuria.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.