Evidence map›Paper›PMID 26787506›Full record

ArticleBritish journal of pharmacology2016

Fenofibrate inhibits atrial metabolic remodelling in atrial fibrillation through PPAR-α/sirtuin 1/PGC-1α pathway.

Guang-Zhong Liu, Ting-Ting Hou, Yue Yuan, Peng-Zhou Hang, Jing-Jing Zhao, Li Sun, Guan-Qi Zhao, Jing Zhao, Jing-Mei Dong, Xiao-Bing Wang and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.7field-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

60 citing papers in PubMed, 91 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Metformin Protects Against Persistent Atrial Fibrillation in an Equine Model.Circulation. Arrhythmia and electrophysiology · 2025
    Article
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  20. Heliyon · 2024
    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

18 authors at 3 institutions in 1 country.

Guang-Zhong LiuDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Ting-Ting HouDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Yue YuanDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Peng-Zhou HangInstitute of Clinical Pharmacology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Jing-Jing ZhaoDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Li SunDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Guan-Qi ZhaoDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Jing ZhaoKey Laboratory of Cardiac Diseases and Heart, Failure of Harbin Medical University, Harbin, Heilongjiang Province, China.
Jing-Mei DongDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Xiao-Bing WangDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Hang ShiDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Yong-Wu LiuCentre for Drug Safety Evaluation, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang Province, China.
Jing-Hua ZhouDepartment of Morphology, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang Province, China.
Zeng-Xiang DongKey Laboratory of Cardiac Diseases and Heart, Failure of Harbin Medical University, Harbin, Heilongjiang Province, China.
Yang LiuDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Cheng-Chuang ZhanDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Yue LiDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Wei-Min LiDepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Harbin Medical University · CNFirst Affiliated Hospital of Harbin Medical University · CNHeilongjiang University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeAtrial metabolic remodelling is critical for the process of atrial fibrillation (AF). The PPAR-α/sirtuin 1 /PPAR co-activator α (PGC-1α) pathway plays an important role in maintaining energy metabolism. However, the effect of the PPAR-α agonist fenofibrate on AF is unclear. Therefore, the aim of this study was to determine the effect of fenofibrate on atrial metabolic remodelling in AF and explore its possible mechanisms of action. EXPERIMENTAL APPROACH: The expression of metabolic proteins was examined in the left atria of AF patients. Thirty-two rabbits were divided into sham, AF (pacing with 600 beats·min(-1) for 1 week), fenofibrate treated (pretreated with fenofibrate before pacing) and fenofibrate alone treated (for 2 weeks) groups. HL-1 cells were subjected to rapid pacing in the presence or absence of fenofibrate, the PPAR-α antagonist GW6471 or sirtuin 1-specific inhibitor EX527. Metabolic factors, circulating biochemical metabolites, atrial electrophysiology, adenine nucleotide levels and accumulation of glycogen and lipid droplets were assessed. KEY

resultsThe PPAR-α/sirtuin 1/PGC-1α pathway was significantly inhibited in AF patients and in the rabbit/HL-1 cell models, resulting in a reduction of key downstream metabolic factors; this effect was significantly restored by fenofibrate. Fenofibrate prevented the alterations in circulating biochemical metabolites, reduced the level of adenine nucleotides and accumulation of glycogen and lipid droplets, reversed the shortened atrial effective refractory period and increased risk of AF. CONCLUSION AND IMPLICATIONS: Fenofibrate inhibited atrial metabolic remodelling in AF by regulating the PPAR-α/sirtuin 1/PGC-1α pathway. The present study may provide a novel therapeutic strategy for AF.

Indexed as

AnimalsAtrial FibrillationAtrial RemodelingCarbazolesCell LineFenofibrateHeart AtriaHumansMaleMiddle AgedOxazolesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR alphaRabbitsSirtuin 1Tyrosine6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamideCarbazolesFenofibrateGW 6471OxazolesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR alphaSirtuin 1Tyrosine

Identifiers

PMID26787506
PMCPMC5341245
OpenAlexW2329499664

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.