Evidence map›Paper›PMID 24713422›Full record

ReviewFree radical biology & medicine2014

Mitochondria and arrhythmias.

Kai-Chien Yang, Marcelo G Bonini, Samuel C Dudley

Open access · bronzeAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

79 citing papers in PubMed, 132 citations in OpenAlex.

  1. Article
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  3. Lysosomal CaCirculation. Arrhythmia and electrophysiology · 2025
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19 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Kai-Chien YangLifespan Cardiovascular Institute, Providence VA Medical Center, and Brown University, Providence, RI 02903, USA.
Marcelo G BoniniDepartment of Medicine/Cardiology, University of Illinois at Chicago, Chicago, IL 60612, USA; Department of Pathology, and University of Illinois at Chicago, Chicago, IL 60612, USA; Department of Pharmacology, University of Illinois at Chicago, Chicago, IL 60612, USA.
Samuel C DudleyLifespan Cardiovascular Institute, Providence VA Medical Center, and Brown University, Providence, RI 02903, USA. Electronic address: samuel_dudley@brown.edu.
Brown University · USProvidence VA Medical Center · USUniversity 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
Metabolic Regulation of Sodium ChannelsR01HL106592 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDLEY, SAMUEL C · 2011 to 2014
$1.6M
Oxidative Stress and Left Ventricular Diastolic FunctionR01HL085520 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDLEY, SAMUEL C · 2008 to 2008
$317k
American Heart Association-American Stroke Association 13POST14380029BLRD VA I01 BX000859NHLBI NIH HHS HL106592NHLBI NIH HHS R01 HL085520NHLBI NIH HHS R01 HL104025NHLBI NIH HHS R01HL104025NHLBI NIH HHS R01 HL106592
6 · The paper itself

Abstract

Mitochondria are essential to providing ATP, thereby satisfying the energy demand of the incessant electrical activity and contractile action of cardiac muscle. Emerging evidence indicates that mitochondrial dysfunction can adversely affect cardiac electrical functioning by impairing the intracellular ion homeostasis and membrane excitability through reduced ATP production and excessive reactive oxygen species (ROS) generation, resulting in increased propensity to cardiac arrhythmias. In this review, the molecular mechanisms linking mitochondrial dysfunction to cardiac arrhythmias are discussed with an emphasis on the impact of increased mitochondrial ROS on the cardiac ion channels and transporters that are critical to maintaining normal electromechanical functioning of the cardiomyocytes. The potential of using mitochondria-targeted antioxidants as a novel antiarrhythmia therapy is highlighted.

Indexed as

Adenosine TriphosphateAnimalsAntioxidantsArrhythmias, CardiacCalciumCalcium ChannelsCardiotonic AgentsHumansMitochondria, HeartMyocardiumMyocytes, CardiacOxidation-ReductionPotassium ChannelsReactive Oxygen SpeciesSodium ChannelsAdenosine TriphosphateAntioxidantsCalciumCalcium ChannelsCardiotonic AgentsPotassium ChannelsReactive Oxygen SpeciesSodium ChannelsCalciumFree radicalsHeartIon channelsReactive oxygen speciesSudden death

Identifiers

PMID24713422
PMCPMC4096785
OpenAlexW1997784203

What OpenQuestion holds

Textmetadata
LicenceTDM
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.