Evidence map›Paper›PMID 14694147›Full record

ReviewThe Journal of physiology2004

Xanthine oxidoreductase and cardiovascular disease: molecular mechanisms and pathophysiological implications.

Cristine E Berry, Joshua M Hare

Registry-linked trialOpen access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05414669 (The Effect of Allopurinol on Malondialdehyde, Nitric Oxide, Kidney Injury Molecule-1 Urine Levels, Resistive Index and Renal Elastography in Kidney Stone Patients After Extra Corporeal Shockwave Lithotripsy), which is not on this map. Cited by 339 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
339citing papers in PubMed, 2 pooled it
15.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

NCT05414669 phase4completednot on this mapstarted 2020, after this paper: background citation

The Effect of Allopurinol on Malondialdehyde, Nitric Oxide, Kidney Injury Molecule-1 Urine Levels, Resistive Index and Renal Elastography in Kidney Stone Patients After Extra Corporeal Shockwave Lithotripsy

TypeinterventionalSponsorRSUP Prof. Dr. I.G.N.G. NgoerahalRan2020 to 2021Enrolled35ConditionsKidney CalculiArmsAllopurinol Tablet 300 mg, Control Group
3 · Its place in the literature

Who cites it

339 citing papers in PubMed, 2 syntheses or guidelines pooled it, 922 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
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  7. Review
  8. Article
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  13. A perspective on the future of heart failure research.Journal of molecular and cellular cardiology plus · 2026
    Article
  14. Review
  15. Insights into the biological effects of molybdenum in an insect model (Frontiers in bioengineering and biotechnology · 2026
    Article
  16. Article
  17. The molecular mechanisms and therapeutic implications of PANoptosis in ischemic diseases.Apoptosis : an international journal on programmed cell death · 2025
    Review
  18. Article
  19. Article
  20. Article

279 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Cristine E BerryThe Johns Hopkins Hospital School of Medicine, Cardiology Division, 600 N Wolfe Street, Carnegie 568, Baltimore, MD 21287, USA.
Joshua M Hare
Johns Hopkins Hospital · US

Funding

OXIDATIVE STRESS IN HEART FAILURE: MECHANISMSR01HL065455 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2000 to 2008
$2.6M
NHLBI NIH HHS R01 HL-065455NHLBI NIH HHS R01 HL065455
6 · The paper itself

Abstract

There is substantial evidence that oxidative stress participates in the pathophysiology of cardiovascular disease. Biochemical, molecular and pharmacological studies further implicate xanthine oxidoreductase (XOR) as a source of reactive oxygen species in the cardiovascular system. XOR is a member of the molybdoenzyme family and is best known for its catalytic role in purine degradation, metabolizing hypoxanthine and xanthine to uric acid with concomitant generation of superoxide. Gene expression of XOR is regulated by oxygen tension, cytokines and glucocorticoids. XOR requires molybdopterin, iron-sulphur centres, and FAD as cofactors and has two interconvertible forms, xanthine oxidase and xanthine dehydrogenase, which transfer electrons from xanthine to oxygen and NAD(+), respectively, yielding superoxide, hydrogen peroxide and NADH. Additionally, XOR can generate superoxide via NADH oxidase activity and can produce nitric oxide via nitrate and nitrite reductase activities. While a role for XOR beyond purine metabolism was first suggested in ischaemia-reperfusion injury, there is growing awareness that it also participates in endothelial dysfunction, hypertension and heart failure. Importantly, the XOR inhibitors allopurinol and oxypurinol attenuate dysfunction caused by XOR in these disease states. Attention to the broader range of XOR bioactivity in the cardiovascular system has prompted initiation of several randomised clinical outcome trials, particularly for congestive heart failure. Here we review XOR gene structure and regulation, protein structure, enzymology, tissue distribution and pathophysiological role in cardiovascular disease with an emphasis on heart failure.

Indexed as

AnimalsCardiovascular DiseasesGene ExpressionGene Expression RegulationHumansProtein Structure, SecondaryProtein Structure, TertiaryTissue DistributionXanthine DehydrogenaseXanthine OxidaseXanthine DehydrogenaseXanthine Oxidase

Identifiers

PMID14694147
PMCPMC1664875
OpenAlexW1953423403

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.