Evidence map›Paper›PMID 37891912›Full record

ReviewAntioxidants (Basel, Switzerland)2023

NADPH Oxidases and Oxidative Stress in the Pathogenesis of Atrial Fibrillation.

Roberto Ramos-Mondragón, Andrey Lozhkin, Aleksandr E Vendrov, Marschall S Runge, Lori L Isom, Nageswara R Madamanchi

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 3 pooled it
11.9field-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.

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

42 citing papers in PubMed, 3 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Lipopeptides fromBiotech (Basel (Switzerland)) · 2026
    Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Gene Therapies in Atrial Fibrillation.Journal of cardiovascular translational research · 2025
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review
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

6 authors at 1 institution in 1 country.

Roberto Ramos-MondragónDepartment of Pharmacology, University of Michigan, 1150 West Medical Center Drive, 2301 Medical Science Research Building III, Ann Arbor, MI 48109, USA.
Andrey LozhkinDepartment of Internal Medicine, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, MI 48019, USA.ORCID 0000-0002-1604-1603
Aleksandr E VendrovDepartment of Internal Medicine, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, MI 48019, USA.
Marschall S RungeDepartment of Internal Medicine, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, MI 48019, USA.
Lori L IsomDepartment of Pharmacology, University of Michigan, 1150 West Medical Center Drive, 2301 Medical Science Research Building III, Ann Arbor, MI 48109, USA.
Nageswara R MadamanchiDepartment of Internal Medicine, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, MI 48019, USA.ORCID 0000-0003-0590-0908
University of Michigan · US

Funding

Cardiac Mechanisms of Sudden Unexpected Death in EpilepsyR01HL149363 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ISOM, LORI L., PARENT, JACK M · 2020 to 2023
$2.8M
NHLBI NIH HHS R01 HL149363
6 · The paper itself

Abstract

Atrial fibrillation (AF) is the most common type of cardiac arrhythmia and its prevalence increases with age. The irregular and rapid contraction of the atria can lead to ineffective blood pumping, local blood stasis, blood clots, ischemic stroke, and heart failure. NADPH oxidases (NOX) and mitochondria are the main sources of reactive oxygen species in the heart, and dysregulated activation of NOX and mitochondrial dysfunction are associated with AF pathogenesis. NOX- and mitochondria-derived oxidative stress contribute to the onset of paroxysmal AF by inducing electrophysiological changes in atrial myocytes and structural remodeling in the atria. Because high atrial activity causes cardiac myocytes to expend extremely high energy to maintain excitation-contraction coupling during persistent AF, mitochondria, the primary energy source, undergo metabolic stress, affecting their morphology, Ca

Indexed as

agingarrhythmiacardiomyocytecell signalingelectrical remodelingmitochondrial oxidative stressNADPH oxidasesNOX1NOX2NOX4paroxysmal atrial fibrillationpermanent atrial fibrillationRac1reentryROSstructural remodelingtachypacing

Identifiers

PMID37891912
PMCPMC10604902
OpenAlexW4387400114

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.