Evidence map›Paper›PMID 27536244›Full record

ReviewFrontiers in physiology2016

Reactive Oxygen Species, Endoplasmic Reticulum Stress and Mitochondrial Dysfunction: The Link with Cardiac Arrhythmogenesis.

Gary Tse, Bryan P Yan, Yin W F Chan, Xiao Yu Tian, Yu Huang

Abstract readReview
In one paragraph

Review in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 5 pooled it
–field-weighted citation impact
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

86 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
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  14. Mitochondrial dysfunction as a central hub linking NaFrontiers in cardiovascular medicine · 2025
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  15. Article
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  19. Article
  20. Progress of uric acid in cardiovascular disease.Cardiovascular endocrinology & metabolism · 2024
    Review

26 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

5 authors.

Gary TseLi Ka Shing Faculty of Medicine, School of Biomedical Sciences, University of Hong KongHong Kong, China; Department of Medicine and Therapeutics, Faculty of Medicine, Chinese University of Hong KongHong Kong, China.
Bryan P YanDepartment of Medicine and Therapeutics, Faculty of Medicine, Chinese University of Hong KongHong Kong, China; Department of Epidemiology and Preventive Medicine, Monash UniversityMelbourne, VIC, Australia.
Yin W F ChanDepartment of Psychology, School of Biological Sciences, University of Cambridge Cambridge, UK.
Xiao Yu TianFaculty of Medicine, School of Biomedical Sciences, Chinese University of Hong Kong Hong Kong, China.
Yu HuangFaculty of Medicine, School of Biomedical Sciences, Chinese University of Hong Kong Hong Kong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiac arrhythmias represent a significant problem globally, leading to cerebrovascular accidents, myocardial infarction, and sudden cardiac death. There is increasing evidence to suggest that increased oxidative stress from reactive oxygen species (ROS), which is elevated in conditions such as diabetes and hypertension, can lead to arrhythmogenesis.

methodA literature review was undertaken to screen for articles that investigated the effects of ROS on cardiac ion channel function, remodeling and arrhythmogenesis.

resultsProlonged endoplasmic reticulum stress is observed in heart failure, leading to increased production of ROS. Mitochondrial ROS, which is elevated in diabetes and hypertension, can stimulate its own production in a positive feedback loop, termed ROS-induced ROS release. Together with activation of mitochondrial inner membrane anion channels, it leads to mitochondrial depolarization. Abnormal function of these organelles can then activate downstream signaling pathways, ultimately culminating in altered function or expression of cardiac ion channels responsible for generating the cardiac action potential (AP). Vascular and cardiac endothelial cells become dysfunctional, leading to altered paracrine signaling to influence the electrophysiology of adjacent cardiomyocytes. All of these changes can in turn produce abnormalities in AP repolarization or conduction, thereby increasing likelihood of triggered activity and reentry.

conclusionROS plays a significant role in producing arrhythmic substrate. Therapeutic strategies targeting upstream events include production of a strong reducing environment or the use of pharmacological agents that target organelle-specific proteins and ion channels. These may relieve oxidative stress and in turn prevent arrhythmic complications in patients with diabetes, hypertension, and heart failure.

Indexed as

arrhythmiaconductionendoplasmic reticulummitochondriaoxidative stressreactive oxygen speciesremodelingrepolarization

Identifiers

PMID27536244
PMCPMC4971160

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Registered trials

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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.