Evidence map›Paper›PMID 31431066›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2019

Contribution of DNA methylation in chronic stress-induced cardiac remodeling and arrhythmias in mice.

Peng Zhang, Tao Li, Ya-Qin Liu, Hao Zhang, Si-Meng Xue, Guang Li, Hai-Ying Mary Cheng, Ji-Min Cao

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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  11. Cardiomyopathies in China: A 2018-2019 state-of-the-art review.Chronic diseases and translational medicine · 2020
    Review
  12. Epitranscriptomics in the Heart: a Focus on mCurrent heart failure reports · 2020
    Review
  13. Article
  14. 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 2 institutions in 2 countries.

Peng Zhang *Institute of Cardiovascular Research, Key Laboratory of Medical Electrophysiology, Ministry of Education-Medical Electrophysiological Key Laboratory of Sichuan Province, Southwest Medical University, Luzhou, China.
Tao Li *Institute of Cardiovascular Research, Key Laboratory of Medical Electrophysiology, Ministry of Education-Medical Electrophysiological Key Laboratory of Sichuan Province, Southwest Medical University, Luzhou, China.
Ya-Qin Liu *Institute of Cardiovascular Research, Key Laboratory of Medical Electrophysiology, Ministry of Education-Medical Electrophysiological Key Laboratory of Sichuan Province, Southwest Medical University, Luzhou, China.
Hao ZhangInstitute of Cardiovascular Research, Key Laboratory of Medical Electrophysiology, Ministry of Education-Medical Electrophysiological Key Laboratory of Sichuan Province, Southwest Medical University, Luzhou, China.
Si-Meng XueInstitute of Cardiovascular Research, Key Laboratory of Medical Electrophysiology, Ministry of Education-Medical Electrophysiological Key Laboratory of Sichuan Province, Southwest Medical University, Luzhou, China.
Guang LiInstitute of Cardiovascular Research, Key Laboratory of Medical Electrophysiology, Ministry of Education-Medical Electrophysiological Key Laboratory of Sichuan Province, Southwest Medical University, Luzhou, China.
Hai-Ying Mary ChengDepartment of Biology, University of Toronto Mississauga, Mississauga, Ontario, Canada.
Ji-Min CaoInstitute of Cardiovascular Research, Key Laboratory of Medical Electrophysiology, Ministry of Education-Medical Electrophysiological Key Laboratory of Sichuan Province, Southwest Medical University, Luzhou, China.
Southwest Medical University · CNUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is recognized that stress can induce cardiac dysfunction, but the underlying mechanisms are not well understood. The present study aimed to test the hypothesis that chronic negative stress leads to alterations in DNA methylation of certain cardiac genes, which in turn contribute to pathologic remodeling of the heart. We found that mice that were exposed to chronic restraint stress (CRS) for 4 wk exhibited cardiac remodeling toward heart failure, as characterized by ventricular chamber dilatation, wall thinning, and decreased contractility. CRS also induced cardiac arrhythmias, including intermittent sinus tachycardia and bradycardia, frequent premature ventricular contraction, and sporadic atrioventricular conduction block. Circulating levels of stress hormones were elevated, and the cardiac expression of tyrosine hydroxylase, a marker of sympathetic innervation, was increased in CRS mice. Using reduced representation bisulfite sequencing, we found that although CRS did not lead to global changes in DNA methylation in the murine heart, it nevertheless altered methylation at specific genes that are associated with the dilated cardiomyopathy (DCM) (

Indexed as

DNA MethylationAnimalsArrhythmias, CardiacChronic DiseaseHeartHeart FailureMaleMiceMice, Inbred C57BLReceptors, Adrenergic, alpha-1Stress, PsychologicalVentricular RemodelingReceptors, Adrenergic, alpha-1cardiovascular diseaseschronic restraint stressreduced representation bisulfite sequencing

Identifiers

PMID31431066
PMCPMC6902688
OpenAlexW2969675319

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.