Evidence map›Paper›PMID 19273066›Full record

ReviewFrontiers in bioscience (Landmark edition)2009

Role of xanthine oxidoreductase in cardiac nitroso-redox imbalance.

Konstantinos Tziomalos, Joshua M Hare

Open access · bronzeAbstract readReview
In one paragraph

Review in Frontiers in bioscience (Landmark edition), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 16% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. Prenylcysteine Oxidase 1 Deficiency Protects the Cardiac Muscle Cell Line HL-1 Against Ischaemic/Hypoxic Stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. The NO/ONOO-cycle as the central cause of heart failure.International journal of molecular sciences · 2013
    Review
  7. Nitric oxide synthases in heart failure.Antioxidants & redox signaling · 2013
    Review
  8. Article
  9. Article
  10. Article
  11. Redox signaling in cardiac myocytes.Free radical biology & medicine · 2011
    Review
  12. Article
  13. Article
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.

Konstantinos TziomalosInterdisciplinary Stem Cell Institute and Division of Cardiology, Leonard M. Miller School of Medicine, University of Miami, Miami, FL, USA.
Joshua M Hare
University of Miami · US

Funding

Mesenchymal Stem Cell CardiomyoplastyU54HL081028 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI HARE, JOSHUA M · 2005 to 2009
$12.1M
Cellular Cardiomyoplasty for Chronic Heart FailureR01HL084275 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2007 to 2016
$3.8M
OXIDATIVE STRESS IN HEART FAILURE: MECHANISMSR01HL065455 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2000 to 2008
$2.6M
Aging impairs stem-cell mediated myocardial repairR01AG025017 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2004 to 2008
$1.5M
NHLBI NIH HHS 2R01 HL-65455-05NHLBI NIH HHS R01 HL065455NHLBI NIH HHS R01 HL084275NHLBI NIH HHS R01HL084275NHLBI NIH HHS U54 HL081028NHLBI NIH HHS U54HL081028-01NIA NIH HHS R01 AG025017
6 · The paper itself

Abstract

Emerging evidence supports the importance of nitroso-redox balance in the cardiovascular system. Xanthine oxidoreductase (XOR) is a major oxidative enzyme and increased XOR activity, leading to both increased production of reactive oxygen species and uric acid, is implicated in heart failure. Within the heart, XOR activity stimulates cardiomyocyte hypertrophy, apoptosis, and impairs matrix structure. The underpinnings of these derangements can be linked not solely to oxidative stress, but may also involve the process of nitroso-redox imbalance. In this regard, XOR interacts with nitric oxide signaling at numerous levels, including a direct protein-protein interaction with neuronal nitric oxide synthase (NOS1) in the sarcoplasmic reticulum. Deficiency or translocation of NOS1 away from this microdomain leads to increased activity of XOR, which in turn impairs excitation-contraction coupling and myofilament calcium sensitivity. There is a mounting abundance of preclinical data supporting beneficial effects of inhibiting XOR, but translation to the clinic continues to be incomplete. A growing understanding of XOR and its role in nitroso-redox imbalance has great potential to lead to improved pathophysiologic insights and possibly therapeutic advances.

Indexed as

AdipocytesAnimalsAntioxidantsHumansMyocardial ContractionMyocardial IschemiaMyocardiumNitrosationOxidation-ReductionReactive Oxygen SpeciesXanthine DehydrogenaseAntioxidantsReactive Oxygen SpeciesXanthine Dehydrogenase

Identifiers

PMID19273066
PMCPMC4745900
OpenAlexW1991891990

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.