Evidence map›Paper›PMID 31415862›Full record

ArticleJournal of cardiac failure2019

Molecular Mechanism of the Association Between Atrial Fibrillation and Heart Failure Includes Energy Metabolic Dysregulation Due to Mitochondrial Dysfunction.

Cevher Ozcan, Zhenping Li, Gene Kim, Valluvan Jeevanandam, Nir Uriel

Open access · greenAbstract read
In one paragraph

Article in Journal of cardiac failure, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 62 citations in OpenAlex.

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  12. Oxidative stress and atrial fibrillation.Journal of molecular and cellular cardiology · 2024
    Review
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  19. Article
  20. Targeting Autophagy in Atrial Fibrillation.Reviews in cardiovascular medicine · 2023
    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

5 authors at 1 institution in 1 country.

Cevher OzcanDepartment of Medicine, Section of Cardiology, University of Chicago Medical Center, Chicago, Illinois. Electronic address: cozcan@uchicago.edu.
Zhenping LiDepartment of Medicine, Section of Cardiology, University of Chicago Medical Center, Chicago, Illinois.
Gene KimDepartment of Medicine, Section of Cardiology, University of Chicago Medical Center, Chicago, Illinois.
Valluvan JeevanandamDepartment of Medicine, Section of Cardiology, University of Chicago Medical Center, Chicago, Illinois; Department of Surgery, Section of Cardiac and Thoracic Surgery, Heart and Vascular Center, University of Chicago Medical Center, Chicago, Illinois.
Nir UrielDepartment of Medicine, Section of Cardiology, University of Chicago Medical Center, Chicago, Illinois.
University of Chicago Medical Center · US

Funding

Mitochondrial Mechanisms and Novel Therapeutic Targets in Atrial FibrillationK08HL117082 · NHLBI · UNIVERSITY OF CHICAGO · PI OZCAN, CEVHER · 2014 to 2018
$798k
NHLBI NIH HHS K08 HL117082
6 · The paper itself

Abstract

backgroundAtrial fibrillation (AF) and heart failure (HF) commonly coexist, yet the molecular mechanisms of this association have not been determined. We hypothesized that an energy deficit due to mitochondrial dysfunction plays a significant role in pathogenic link between AF and HF. METHODS AND

resultsMyocardial energy metabolism and mitochondria were examined in atrial tissue samples from patients and mice (cardiac-specific LKB1 knock-out) with HF and/or AF. There was significant atrial energy (ATP) deficit in patients with HF (11.5±1.3 nmol/mg, n=10; vs without HF 17±3.8 nmol/mg, n=5, P = .032). AF was associated with further energy depletion (ATP 5.4±1.2 nmol/mg, n=9) in HF (P = .001) and metabolic stress (AMP/ATP 1.6±0.1 vs 0.7±0.2 in HF alone; P = .043). The left atrium demonstrated lower ATP than the right (P = .004). Mitochondrial dysfunction and remodeling caused ATP depletion with impaired oxidative phosphorylation complexes (succinate dehydrogenase and cytochrome c oxidase), increased reactive oxygen species, and mtDNA damage in mice and human atria with AF and HF.

conclusionsMolecular mechanisms of the association between HF and AF include an energy deficit due to mitochondrial dysfunction in atrial myocardium. Mitochondrial functional and structural remodeling in human and mouse atria is associated with energy metabolic dysregulation and oxidative stress that promote AF in HF and vice versa.

Indexed as

AdultAnimalsAtrial FibrillationElectron Transport Complex IVEnergy MetabolismFemaleHeart AtriaHeart FailureHumansMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMiddle AgedMitochondriaElectron Transport Complex IVSuccinate DehydrogenaseAtrial fibrillationenergy metabolismheart failuremitochondria

Identifiers

PMID31415862
PMCPMC7144800
OpenAlexW2967488641

What OpenQuestion holds

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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.