Evidence map›Paper›PMID 32879139›Full record

ArticleJCI insight2020

Apelin increases atrial conduction velocity, refractoriness, and prevents inducibility of atrial fibrillation.

Young M Kim, Robert Lakin, Hao Zhang, Jack Liu, Ayaaz Sachedina, Maneesh Singh, Emily Wilson, Marco Perez, Subodh Verma, Thomas Quertermous and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. The Impact of the Apelinergic System on the Cardiovascular System.International journal of molecular sciences · 2025
    Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Observational
  11. Article
  12. Article
  13. Review
  14. 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

13 authors at 4 institutions in 2 countries.

Young M KimDivision of Cardiovascular Medicine, Stanford Medicine, Stanford, California, USA.
Robert LakinDepartment of Biology, York University, Toronto, Ontario, Canada.
Hao ZhangDivision of Cardiovascular Medicine, University of California, San Francisco, San Francisco, California, USA.
Jack LiuDivision of Cardiology, University Health Network, Toronto, Ontario, Canada.
Ayaaz SachedinaDivision of Cardiology, University Health Network, Toronto, Ontario, Canada.
Maneesh SinghDivision of Cardiovascular Medicine, Stanford Medicine, Stanford, California, USA.
Emily WilsonDivision of Cardiovascular Medicine, University of California, San Francisco, San Francisco, California, USA.
Marco PerezDivision of Cardiovascular Medicine, Stanford Medicine, Stanford, California, USA.
Subodh VermaDepartment of Biology, York University, Toronto, Ontario, Canada.
Thomas QuertermousDivision of Cardiovascular Medicine, Stanford Medicine, Stanford, California, USA.
Jeffrey OlginDivision of Cardiovascular Medicine, University of California, San Francisco, San Francisco, California, USA.
Peter H BackxDepartment of Biology, York University, Toronto, Ontario, Canada.
Euan A AshleyDivision of Cardiovascular Medicine, Stanford Medicine, Stanford, California, USA.
Stanford Medicine · USUniversity Health Network · CAUniversity of California, San Francisco · USYork University · CA

Funding

CIHR MOP-119339CIHR MOP125950CIHR MOP-83453
6 · The paper itself

Abstract

Previous studies have shown an association between elevated atrial NADPH-dependent oxidative stress and decreased plasma apelin in patients with atrial fibrillation (AF), though the basis for this relationship is unclear. In the current study, RT-PCR and immunofluorescence studies of human right atrial appendages (RAAs) showed expression of the apelin receptor, APJ, and reduced apelin content in the atria, but not in plasma, of patients with AF versus normal sinus rhythm. Disruption of the apelin gene in mice increased (2.4-fold) NADPH-stimulated superoxide levels and slowed atrial conduction velocities in optical mapping of a Langendorff-perfused isolated heart model, suggesting that apelin levels may influence AF vulnerability. Indeed, in mice with increased AF vulnerability (induced by chronic intense exercise), apelin administration reduced the incidence and duration of induced atrial arrhythmias in association with prolonged atrial refractory periods. Moreover, apelin decreased AF induction in isolated atria from exercised mice while accelerating conduction velocity and increasing action potential durations. At the cellular level, these changes were associated with increased atrial cardiomyocyte sodium currents. These findings support the conclusion that reduced atrial apelin is maladaptive in fibrillating human atrial myocardium and that increasing apelin bioavailability may be a worthwhile therapeutic strategy for treating and preventing AF.

Indexed as

Atrial FunctionAction PotentialsAgedAnimalsApelinApelin ReceptorsAtrial FibrillationCells, CulturedFemaleHeart AtriaHeart RateHumansMaleMiceMiddle AgedMyocytes, CardiacApelinApelin ReceptorsAPLN protein, humanArrhythmiasCardiology

Identifiers

PMID32879139
PMCPMC7526452
OpenAlexW3082543680

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.