Evidence map›Paper›PMID 26786158›Full record

ReviewCardiovascular research2016

Compromised redox homeostasis, altered nitroso-redox balance, and therapeutic possibilities in atrial fibrillation.

Jillian N Simon, Klemen Ziberna, Barbara Casadei

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Oxidative stress and atrial fibrillation.Journal of molecular and cellular cardiology · 2024
    Review
  5. Review
  6. Advances in basic and translational research in atrial fibrillation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Ion Channel and Structural Remodeling in Obesity-Mediated Atrial Fibrillation.Circulation. Arrhythmia and electrophysiology · 2020
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  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

3 authors at 1 institution in 1 country.

Jillian N SimonRadcliffe Department of Medicine, Division of Cardiovascular Medicine, University of Oxford, Oxford, UK.
Klemen ZibernaRadcliffe Department of Medicine, Division of Cardiovascular Medicine, University of Oxford, Oxford, UK.
Barbara CasadeiRadcliffe Department of Medicine, Division of Cardiovascular Medicine, University of Oxford, Oxford, UK barbara.casadei@cardiov.ox.ac.uk.
University of Oxford · GB

Funding

British Heart Foundation CH/12/3/29609British Heart Foundation RG/11/15/29375Medical Research Council
6 · The paper itself

Abstract

Although the initiation, development, and maintenance of atrial fibrillation (AF) have been linked to alterations in myocyte redox state, the field lacks a complete understanding of the impact these changes may have on cellular signalling, atrial electrophysiology, and disease progression. Recent studies demonstrate spatiotemporal changes in reactive oxygen species production shortly after the induction of AF in animal models with an uncoupling of nitric oxide synthase activity ensuing in the presence of long-standing persistent AF, ultimately leading to a major shift in nitroso-redox balance. However, it remains unclear which radical or non-radical species are primarily involved in the underlying mechanisms of AF or which proteins are targeted for redox modification. In most instances, only free radical oxygen species have been assessed; yet evidence from the redox signalling field suggests that non-radical species are more likely to regulate cellular processes. A wider appreciation for the distinction of these species and how both species may be involved in the development and maintenance of AF could impact treatment strategies. In this review, we summarize how redox second-messenger systems are regulated and discuss the recent evidence for alterations in redox regulation in the atrial myocardium in the presence of AF, while identifying some critical missing links. We also examine studies looking at antioxidants for the prevention and treatment of AF and propose alternative redox targets that may serve as superior therapeutic options for the treatment of AF.

Indexed as

AnimalsAntioxidantsAtrial FibrillationHeart AtriaHomeostasisHumansOxidation-ReductionReactive Oxygen SpeciesAntioxidantsReactive Oxygen SpeciesAntioxidantsArrhythmiaHeartHydrogen peroxideNitric oxideSubcellular localization

Identifiers

PMID26786158
PMCPMC4777914
OpenAlexW2270047458

What OpenQuestion 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 OpenQuestion graph.