Evidence map›Paper›PMID 23241320›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2013

Impact of glucose-6-phosphate dehydrogenase deficiency on the pathophysiology of cardiovascular disease.

Peter A Hecker, Jane A Leopold, Sachin A Gupte, Fabio A Recchia, William C Stanley

Abstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 3% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. NADPCurrent medicinal chemistry · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

5 authors at 4 institutions in 2 countries.

Peter A HeckerDivision of Cardiology and Department of Medicine, University of Maryland, Baltimore, MD, USA.
Jane A Leopold
Sachin A Gupte
Fabio A Recchia
William C Stanley
University of Maryland, Baltimore · USBrigham and Women's Hospital · USTemple University · USUniversity of South Alabama · US

Funding

Substrate Selection and Oxidative Stress in Heart FailureP01HL074237 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI STANLEY, WILLIAM C · 2003 to 2013
$19.9M
JHU-UMD Diabetes Research CenterP30DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI AHIMA, REXFORD S. · 2013 to 2017
$9.7M
Training Grant in Cardiac and Vascular Cell BiologyT32HL072751 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI FISHER, STEVEN A. · 2003 to 2013
$3.1M
Aldosterone, Autophagy, and Arterial StiffnessR01HL105301 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LEOPOLD, JANE A · 2010 to 2013
$1.6M
VEGF receptor-1-mediated protection in dilated cardiomyopathyR01HL108213 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI RECCHIA, FABIO A · 2012 to 2015
$1.6M
NHLBI NIH HHS HL-105301NHLBI NIH HHS P01-HL-074237NHLBI NIH HHS R01 HL105301NHLBI NIH HHS R01 HL108213NHLBI NIH HHS T32-HL-072751NIDDK NIH HHS P30 DK079637
6 · The paper itself

Abstract

Glucose-6-phosphate dehydrogenase (G6PD) catalyzes the rate-determining step in the pentose phosphate pathway and produces NADPH to fuel glutathione recycling. G6PD deficiency is the most common enzyme deficiency in humans and affects over 400 million people worldwide; however, its impact on cardiovascular disease is poorly understood. The glutathione pathway is paramount to antioxidant defense, and G6PD-deficient cells do not cope well with oxidative damage. Limited clinical evidence indicates that G6PD deficiency may be associated with hypertension. However, there are also data to support a protective role of G6PD deficiency in decreasing the risk of heart disease and cardiovascular-associated deaths, perhaps through a decrease in cholesterol synthesis. Studies in G6PD-deficient (G6PDX) mice are mixed and provide evidence for both protective and deleterious effects. G6PD deficiency may provide a protective effect through decreasing cholesterol synthesis, superoxide production, and reductive stress. However, recent studies indicate that G6PDX mice are moderately more susceptible to ventricular dilation in response to myocardial infarction or pressure overload-induced heart failure. Furthermore, G6PDX hearts do not recover as well as nondeficient mice when faced with ischemia-reperfusion injury, and G6PDX mice are susceptible to the development of age-associated cardiac hypertrophy. Overall, the limited available data indicate a complex interplay in which adverse effects of G6PD deficiency may outweigh potential protective effects in the face of cardiac stress. Definitive clinical studies in large populations are needed to determine the effects of G6PD deficiency on the development of cardiovascular disease and subsequent outcomes.

Indexed as

AnimalsCardiovascular DiseasesEndothelium, VascularFemaleGlucosephosphate Dehydrogenase DeficiencyHeartHumansMaleMiceMutationMyocardiumOxidative StressRatsReperfusion InjurySuperoxidesThiamineSuperoxidesThiamine

Identifiers

PMID23241320
PMCPMC3566485
OpenAlexW2104712114

What OpenQuestion holds

Textmetadata
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.