ArticleOxidative medicine and cellular longevity2016
Lower Superoxide Dismutase 2 (SOD2) Protein Content in Mononuclear Cells Is Associated with Better Survival in Patients with Hemodialysis Therapy.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- PROGRESS Study: Longitudinal analysis of antioxidant status and its relationship with heat shock proteins in children with chronic kidney disease.Pediatric nephrology (Berlin, Germany) · 2026Article
- Vascular Calcification in Chronic Kidney Disease and Hemodialysis: Pathophysiological Mechanisms and Emerging Biomarkers.Medicina (Kaunas, Lithuania) · 2025Review
- The Clinical Utility and Plausibility of Oxidative and Antioxidant Variables in Chronic and End-Stage Kidney Disease: A Review of the Literature.International journal of molecular sciences · 2025Review
- miR-122-5p Regulates Renal Fibrosis In Vivo.International journal of molecular sciences · 2022Article
- Nrf2 Activation in Chronic Kidney Disease: Promises and Pitfalls.Antioxidants (Basel, Switzerland) · 2022Review
- Involvement of Inflammasome Components in Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Endothelial superoxide dismutase 2 is decreased in sickle cell disease and regulates fibronectin processing.Function (Oxford, England) · 2022Article
- Hemodialysis raises oxidative stress through carbon-centered radicals despite improved biocompatibility.Journal of clinical biochemistry and nutrition · 2021Article
- Chronic Kidney Disease as Oxidative Stress- and Inflammatory-Mediated Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Monocytes in Uremia.Toxins · 2020Review
- Article
- Expression of theOxidative medicine and cellular longevity · 2017Article
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial superoxide dismutase 2 (SOD2) converts superoxide anions to hydrogen peroxide and oxygen. Human data on SOD2 protein content in chronic kidney disease (CKD) are sparse and mortality data are lacking. We investigated SOD2 protein content in monocytes from patients with hemodialysis therapy (n = 81), CKD stage 1-5 (n = 120), and healthy controls (n = 13) using in-cell Western assays. SOD2 protein decreased from CKD stage 1 until stage 4 whereas it increased again in stage 5 with and without hemodialysis. SOD2 gene expression, analyzed by quantitative real-time PCR, was not significantly different between the groups. Elevating cellular superoxide production reduced SOD2 protein content. This effect was abolished by the superoxide dismutase mimetic Tempol. Using gelelectrophoresis and Western blot we did not detect nitrotyrosine modifications of SOD2 in CKD. Finally, in patients with CKD stage 5 with hemodialysis therapy higher than median SOD2 protein content was associated with higher all-cause mortality. In conclusion, SOD2 protein content declined in CKD until stage 4 while SOD2 gene expression did not. Increased cellular superoxide anion production might affect SOD2 protein content. In advanced CKD (stage 5) SOD2 protein content increased again, but higher than median SOD2 protein content in these patients did not confer a survival benefit.
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