Evidence map›Paper›PMID 26274906›Full record

ArticlePloS one2015

Free Fatty Acid Effects on the Atrial Myocardium: Membrane Ionic Currents Are Remodeled by the Disruption of T-Tubular Architecture.

Ryan P O'Connell, Hassan Musa, Mario San Martin Gomez, Uma Mahesh Avula, Todd J Herron, Jerome Kalifa, Justus M B Anumonwo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. 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
2.1field-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

24 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. [Overwork damages myocardial energy metabolism homeostasis in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  3. Review
  4. Review
  5. Obesity Arrhythmias: Role of IL-6 Trans-Signaling.International journal of molecular sciences · 2024
    Review
  6. Review
  7. Review
  8. Impact of Obesity on Atrial Electrophysiological Substrate.Journal of cardiovascular development and disease · 2023
    Review
  9. Review
  10. Article
  11. Epicardial adipose tissue as a mediator of cardiac arrhythmias.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  12. Macrophage-Dependent Interleukin-6-Production and Inhibition ofInternational journal of molecular sciences · 2021
    Article
  13. Neurological Disorders and Risk of Arrhythmia.International journal of molecular sciences · 2020
    Review
  14. Differential Modulation ofFrontiers in physiology · 2019
    Article
  15. Article
  16. Metabolic Effects of Metformin in the Failing Heart.International journal of molecular sciences · 2018
    Review
  17. Review
  18. Article
  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

7 authors at 1 institution in 1 country.

Ryan P O'ConnellDepartment of Internal Medicine, Center for Arrhythmia Research, University of Michigan Medical School, Ann Arbor, MI 48109, United States of America; Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, United States of America.
Hassan MusaDepartment of Internal Medicine, Center for Arrhythmia Research, University of Michigan Medical School, Ann Arbor, MI 48109, United States of America.
Mario San Martin GomezDepartment of Internal Medicine, Center for Arrhythmia Research, University of Michigan Medical School, Ann Arbor, MI 48109, United States of America.
Uma Mahesh AvulaDepartment of Internal Medicine, Center for Arrhythmia Research, University of Michigan Medical School, Ann Arbor, MI 48109, United States of America.
Todd J HerronDepartment of Internal Medicine, Center for Arrhythmia Research, University of Michigan Medical School, Ann Arbor, MI 48109, United States of America; Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, United States of America.
Jerome KalifaDepartment of Internal Medicine, Center for Arrhythmia Research, University of Michigan Medical School, Ann Arbor, MI 48109, United States of America.
Justus M B AnumonwoDepartment of Internal Medicine, Center for Arrhythmia Research, University of Michigan Medical School, Ann Arbor, MI 48109, United States of America; Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, United States of America.
University of Michigan–Ann Arbor · US

Funding

Molecular Determinants of Function in Kir2.x channelsR01GM076608 · NIGMS · UPSTATE MEDICAL UNIVERSITY · PI ANUMONWO, JUSTUS M · 2007 to 2011
$1.5M
Arrhythmogenicity of human SAP97 Mutations in patient specific iPSC-CMs and MiceR01HL124319 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ANUMONWO, JUSTUS M · 2015 to 2017
$1.3M
NHLBI NIH HHS R01 HL124319NIGMS NIH HHS 1R01-GM-076608NIGMS NIH HHS R01 GM076608
6 · The paper itself

Abstract

backgroundEpicardial adiposity and plasma levels of free fatty acids (FFAs) are elevated in atrial fibrillation, heart failure and obesity, with potentially detrimental effects on myocardial function. As major components of epicardial fat, FFAs may be abnormally regulated, with a potential to detrimentally modulate electro-mechanical function. The cellular mechanisms underlying such effects of FFAs are unknown.

objectiveTo determine the mechanisms underlying electrophysiological effects of palmitic (PA), stearic (SA) and oleic (OA) FFAs on sheep atrial myocytes.

methodsWe used electrophysiological techniques, numerical simulations, biochemistry and optical imaging to examine the effects of acutely (≤ 15 min), short-term (4-6 hour) or 24-hour application of individual FFAs (10 μM) on isolated ovine left atrial myocytes (LAMs).

resultsAcute and short-term incubation in FFAs resulted in no differences in passive or active properties of isolated left atrial myocytes (LAMs). 24-hour application had differential effects depending on the FFA. PA did not affect cellular passive properties but shortened (p<0.05) action potential duration at 30% repolarization (APD30). APD50 and APD80 were unchanged. SA had no effect on resting membrane potential but reduced membrane capacitance by 15% (p<0.05), and abbreviated APD at all values measured (p≤0.001). OA did not significantly affect passive or active properties of LAMs. Measurement of the major voltage-gated ion channels in SA treated LAMs showed a ~60% reduction (p<0.01) of the L-type calcium current (ICa-L) and ~30% reduction (p<0.05) in the transient outward potassium current (ITO). A human atrial cell model recapitulated SA effects on APD. Optical imaging showed that SA incubated for 24 hours altered t-tubular structure in isolated cells (p<0.0001).

conclusionsSA disrupts t-tubular architecture and remodels properties of membrane ionic currents in sheep atrial myocytes, with potential implications in arrhythmogenesis.

Indexed as

AnimalsCells, CulturedElectrophoresis, Polyacrylamide GelElectrophysiologyFatty Acids, NonesterifiedHeart AtriaImmunoblottingIon TransportMaleMyocardiumSheepFatty Acids, Nonesterified

Identifiers

PMID26274906
PMCPMC4537212
OpenAlexW1771411253

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.