Evidence map›Paper›PMID 28542617›Full record

ArticlePloS one2017

Inflammatory and apoptotic remodeling in autonomic nervous system following myocardial infarction.

Chen Gao, Kimberly Howard-Quijano, Christoph Rau, Tatsuo Takamiya, Yang Song, Kalyanam Shivkumar, Yibin Wang, Aman Mahajan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

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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 1 institution in 1 country.

Chen GaoDivision of Molecular Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, United States of America.
Kimberly Howard-QuijanoDepartment of Anesthesiology and Perioperative Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, United States of America.
Christoph RauDivision of Molecular Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, United States of America.
Tatsuo TakamiyaDepartment of Anesthesiology and Perioperative Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, United States of America.
Yang SongDivision of Molecular Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, United States of America.
Kalyanam ShivkumarUCLA Cardiac Arrhythmia Center, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, United States of America.
Yibin WangDivision of Molecular Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, United States of America.
Aman MahajanDepartment of Anesthesiology and Perioperative Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, United States of America.ORCID http://orcid.org/0000-0003-3853-369X
University of California, Los Angeles · US

Funding

Epigenomic Mechanisms of Heart FailureR01HL129639 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI VONDRISKA, THOMAS M. · 2015 to 2018
$2.6M
Novel Regulatory Circuit in Cardiac Hypertrophy Via RNA SplicingR01HL122737 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, YIBIN · 2014 to 2017
$1.5M
NHLBI NIH HHS R01 HL122737NHLBI NIH HHS R01 HL129639
6 · The paper itself

Abstract

backgroundChronic myocardial infarction (MI) triggers pathological remodeling in the heart and cardiac nervous system. Abnormal function of the autonomic nervous system (ANS), including stellate ganglia (SG) and dorsal root ganglia (DRG) contribute to increased sympathoexcitation, cardiac dysfunction and arrythmogenesis. ANS modulation is a therapeutic target for arrhythmia associated with cardiac injury. However, the molecular mechanism involved in the pathological remodeling in ANS following cardiac injury remains to be established. METHODS AND

resultsIn this study, we performed transcriptome analysis by RNA-sequencing in thoracic SG and (T1-T4) DRG obtained from Yorkshire pigs following either acute (3 to 5 hours) or chronic (8 weeks) myocardial infarction. By differential expression and weighted gene co-expression network analysis (WGCNA), we identified significant transcriptome changes and specific gene modules in the ANS tissues in response to myocardial infarction at either acute or chronic phases. Both differential expressed genes and the member genes of the WGCNA gene module associated with post-infarct condition were significantly enriched for inflammatory signaling and apoptotic cell death. Targeted validation analysis supported a significant induction of inflammatory and apoptotic signal in both SG and DRG following myocardial infarction, along with cellular evidence of apoptosis induction based on TUNEL analysis. Importantly, these molecular changes were observed specifically in the thoracic segments but not in their counterparts obtained from lumbar sections.

conclusionMyocardial injury leads to time-dependent global changes in gene expression in the innervating ANS. Induction of inflammatory gene expression and loss of neuron cell viability in SG and DRG are potential novel mechanisms contributing to abnormal ANS function which can promote cardiac arrhythmia and pathological remodeling in myocardium.

Indexed as

ApoptosisAnimalsGanglia, SpinalGene Expression ProfilingInflammationMaleMyocardial InfarctionStellate GanglionSwine

Identifiers

PMID28542617
PMCPMC5436752
OpenAlexW2620263982

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.