Evidence map›Paper›PMID 19309257›Full record

ReviewAntioxidants & redox signaling2009

Redox regulation, NF-kappaB, and atrial fibrillation.

Ge Gao, Samuel C Dudley

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

45 citing papers in PubMed, 84 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Novel Drug Targets in Diastolic Heart Disease.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Administration of USP7 inhibitor p22077 alleviates Angiotensin II (Ang II)-induced atrial fibrillation in Mice.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  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

2 authors at 1 institution in 1 country.

Ge GaoSection of Cardiology, University of Illinois at Chicago, and the Jesse Brown VA Medical Center, Chicago, Illinois 60612, USA.
Samuel C Dudley
University of Illinois Chicago · US

Funding

Na+ channel mRNA splicing in heart failureR01HL104025 · NHLBI · UNIVERSITY OF MINNESOTA · PI DUDLEY, SAMUEL C · 2011 to 2019
$3.3M
Angiotensin converting enzyme, angiotensin II, and arrhythmiaR01HL085558 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDLEY, SAMUEL C · 2007 to 2010
$1.5M
Stem Cell Therapy and ArrhythmiaR01HL073753 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDLEY, SAMUEL C · 2005 to 2008
$1.4M
Oxidative Stress and Left Ventricular Diastolic FunctionR01HL085520 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDLEY, SAMUEL C · 2008 to 2008
$317k
NHLBI NIH HHS R01 HL073753NHLBI NIH HHS R01 HL085520NHLBI NIH HHS R01 HL085558NHLBI NIH HHS R01 HL104025
6 · The paper itself

Abstract

Atrial fibrillation (AF) is the most common clinically encountered abnormal heart beat. It is associated with an increased risk of stroke and symptoms of heart failure. Current therapies are directed toward controlling the rate of ventricular activation and preventing strokes through anticoagulation. Attempts at suppressing the arrhythmia are often ineffective, in part because the underlying pathogenesis is poorly understood. Recently, structural and electrical remodeling has been shown to occur during AF. These changes involve alterations in gene regulation and help perpetuate the arrhythmia. Some signals for remodeling are have been identified. Moreover, AF is associated with oxidative stress, and this redox imbalance may contribute to the altered gene regulation. One likely mediator of this change in transcriptional regulation is the redox sensitive transcription factor, nuclear factor-kappaB (NF-kappaB). Recently, NF-kappaB has been shown to downregulate transcription of the cardiac sodium channel in response to oxidative stress. NF-kappaB may contribute to the regulation of other ion channels, transcription factors, or splicing factors altered in AF and may represent a therapeutic target in AF management.

Indexed as

Atrial FibrillationGene Expression RegulationHumansNF-kappa BOxidation-ReductionTranscription, GeneticNF-kappa B

Identifiers

PMID19309257
PMCPMC2819799
OpenAlexW1973799448

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.