Evidence map›Paper›PMID 28565869›Full record

ArticleExperimental and therapeutic medicine2017

Mitochondrial dysfunction on sinoatrial node and pulmonary vein electrophysiological activities.

Yung-Kuo Lin, Chen-Chuan Cheng, Min-Chien Tsai, Pei-Yu Wu, Yi-Ann Chen, Yao-Chang Chen, Shih-Ann Chen, Yi-Jen Chen

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

8 authors at 5 institutions in 1 country.

Yung-Kuo LinDivision of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei 110, Taiwan, R.O.C.
Chen-Chuan ChengDivision of Cardiology, Chi-Mei Medical Center, Tainan 710, Taiwan, R.O.C.
Min-Chien TsaiDepartment of Biomedical Engineering and Graduate Institute of Physiology, National Defense Medical Center, Taipei 114, Taiwan, R.O.C.
Pei-Yu WuDepartment of Biomedical Engineering and Graduate Institute of Physiology, National Defense Medical Center, Taipei 114, Taiwan, R.O.C.
Yi-Ann ChenDivision of Nephrology, Sijhih Cathay General Hospital, New Taipei 221, Taiwan, R.O.C.
Yao-Chang ChenDepartment of Biomedical Engineering and Graduate Institute of Physiology, National Defense Medical Center, Taipei 114, Taiwan, R.O.C.
Shih-Ann ChenDivision of Cardiology and Cardiovascular Research Center, Taipei Veterans General Hospitals, National Yang-Ming University School of Medicine, Taipei 112, Taiwan, R.O.C.
Yi-Jen ChenDivision of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei 110, Taiwan, R.O.C.
Cathay General Hospital · TWNational Defense Medical Center · TWChi Mei Medical Center · TWNational Yang Ming Chiao Tung University · TWWan Fang Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrillation (AF) is associated with mitochondrial dysfunction. Sinoatrial node (SAN) dysfunction increases arrhythmogenesis of pulmonary veins (PVs), which is the most important trigger of AF; however, it is not clear whether mitochondrial dysfunction differentially regulates electrical activity of SANs and PVs. In the present study, conventional microelectrodes were used to record the action potentials (APs) in isolated rabbit PVs, SANs, left atrium (LA) and right atrium (RA) before and after application of trifluorocarbonylcyanide phenylhydrazone (FCCP; a mitochondrial uncoupling agent) at 10, 100 and 300 nM. FCCP application at 100 and 300 nM decreased spontaneous rates in PVs and in SANs at 10, 100 and 300 nM. FCCP shortened the 20, 50 and 90% AP durations in the LA, and shortened only the 20% AP duration in the RA. FCCP caused a greater rate reduction in SANs than in PVs; however, in the presence of coenzyme-Q

Indexed as

atrial fibrillationmitochondrial dysfunctionpulmonary veinsinoatrial node

Identifiers

PMID28565869
PMCPMC5443227
OpenAlexW2603383085

What OpenQuestion holds

Textmetadata
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.