ReviewFrontiers in endocrinology2025
Implication of xanthine oxidoreductase in oxidative stress-related chronic diseases.
Review in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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
5 citing papers in PubMed.
- Serum Copper-to-Zinc Ratio and Oxidative Stress Are Associated with Anemia in Older Adults with Cardiovascular-Kidney-Metabolic Syndrome.International journal of molecular sciences · 2026Article
- Understanding Spaceflight-Induced Oxidative Stress and the Critical Role of Diet and Microbiome.Antioxidants (Basel, Switzerland) · 2026Review
- Exploring the relationship between XDH gene variants and serum urate and xanthine dehydrogenase levels in gout.Clinical rheumatology · 2026Article
- Immunometabolic Dysregulation in Preeclampsia: Emerging Roles of Inflammation, Insulin Resistance, Uric Acid, and the Gut Microbiome.Mediators of inflammation · 2026Review
- Hyperuricemia was associated with metabolic response against brain injury instead of metabolism syndrome in Tibet: a cross-sectional analysis.Frontiers in endocrinology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Xanthine oxidoreductase (XOR) catalyzes the final steps of purine catabolism: the oxidation of hypoxanthine to xanthine, and xanthine to UA. XOR exists as interconvertible proteoforms, xanthine dehydrogenase (XDH) and xanthine oxidase (XO). The balance between XDH and XO determines whether purine degradation is redox-neutral or strongly pro-oxidant. Evidence across cardiovascular, renal, oncological and neurological disorders shows that excess XO-derived ROS, rather than UA itself, is a likely mediator of tissue injury and clinical progression, with several lines of research linking them to the interplay between XOR and purinergic signaling. Pharmacological inhibition or down-regulation of XO ameliorates pathology even when UA concentrations remain unchanged, underscoring the therapeutic relevance of the proteoform-specific mechanism. This mini-review focuses on the structure, regulation, and pathological roles of XOR, with emphasis on its implications in oxidative stress-related diseases.
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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 Socratic graph.