Evidence map›Paper›PMID 32409748›Full record

ArticleScientific reports2020

Chronic Sympathetic Hyperactivity Triggers Electrophysiological Remodeling and Disrupts Excitation-Contraction Coupling in Heart.

Humberto C Joca, Artur Santos-Miranda, Julliane V Joviano-Santos, Rebeca P M Maia-Joca, Patricia C Brum, George S B Williams, Jader S Cruz

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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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

7 authors at 4 institutions in 2 countries.

Humberto C JocaDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
Artur Santos-MirandaDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
Julliane V Joviano-SantosDepartment of Biophysics, Universidade Federal de Sao Paulo, Sao Paulo, SP, Brazil.
Rebeca P M Maia-JocaDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
Patricia C BrumSchool of Physical Education and Sport, University of São Paulo, São Paulo, SP, Brazil.
George S B WilliamsCenter for Biomedical Engineering and Technology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Jader S CruzDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil. jcruz@icb.ufmg.br.
Universidade Federal de Minas Gerais · BRUniversidade Federal de São Paulo · BRUniversity of Maryland, Baltimore · USUniversidade de São Paulo · BR

Funding

Mitochondrial Calcium Signaling in HeartK25HL125762 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI WILLIAMS, GEORGE S. B. · 2015 to 2019
$809k
NHLBI NIH HHS K25 HL125762
6 · The paper itself

Abstract

The sympathetic nervous system is essential for maintenance of cardiac function via activation of post-junctional adrenergic receptors. Prolonged adrenergic receptor activation, however, has deleterious long-term effects leading to hypertrophy and the development of heart failure. Here we investigate the effect of chronic adrenergic receptors activation on excitation-contraction coupling (ECC) in ventricular cardiomyocytes from a previously characterized mouse model of chronic sympathetic hyperactivity, which are genetically deficient in the adrenoceptor α2A and α2C genes (ARDKO). When compared to wild-type (WT) cardiomyocytes, ARDKO displayed reduced fractional shortening (~33%) and slower relaxation (~20%). Furthermore, ARDKO cells exhibited several electrophysiological changes such as action potential (AP) prolongation (~50%), reduced L-type calcium channel (LCC) current (~33%), reduced outward potassium (K

Indexed as

Cardiac ElectrophysiologyExcitation Contraction CouplingAlgorithmsAnimalsCalciumCalcium SignalingFluorescent Antibody TechniqueHeart DiseasesMiceModels, BiologicalMyocardiumMyocytes, CardiacSarcoplasmic ReticulumSympathetic Nervous SystemCalcium

Identifiers

PMID32409748
PMCPMC7224293
OpenAlexW3024257323

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.