Evidence map›Paper›PMID 32357113›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2020

Differential effects of REV-ERBα/β agonism on cardiac gene expression, metabolism, and contractile function in a mouse model of circadian disruption.

Sobuj Mia, Mariame S Kane, Mary N Latimer, Cristine J Reitz, Ravi Sonkar, Gloria A Benavides, Samuel R Smith, Stuart J Frank, Tami A Martino, Jianhua Zhang and 2 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  7. Research Progress of BMAL1 in Heart Failure.Journal of the American Heart Association · 2025
    Review
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  10. Circadian biology of cardiac aging.Journal of molecular and cellular cardiology · 2025
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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

12 authors at 2 institutions in 2 countries.

Sobuj MiaDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Mariame S KaneDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Mary N LatimerDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Cristine J ReitzCentre for Cardiovascular Investigations, Department of Biomedical Science, University of Guelph, Guelph, Ontario, Canada.ORCID 0000-0002-1748-0501
Ravi SonkarDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Gloria A BenavidesDivision of Molecular Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama.
Samuel R SmithDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.ORCID 0000-0003-1701-4102
Stuart J FrankDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Tami A MartinoCentre for Cardiovascular Investigations, Department of Biomedical Science, University of Guelph, Guelph, Ontario, Canada.
Jianhua ZhangDivision of Molecular Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama.
Victor M Darley-UsmarDivision of Molecular Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama.
Martin E YoungDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
University of Alabama at Birmingham · USUniversity of Guelph · CA

Funding

Macrophage Circadian Clock Disruption and Inflammation in Heart FailureR01HL147549 · NHLBI · WASHINGTON UNIVERSITY · PI PRABHU, SUMANTH D, YOUNG, MARTIN E · 2019 to 2022
$2.3M
Aberrant Circadian Regulation of Autophagy in the Heart During DiabetesR01HL142216 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C, YOUNG, MARTIN E · 2018 to 2021
$2.3M
Metabolic Rhythm Alterations as a Cause for Obesity CardiomyopathyR01HL149159 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YOUNG, MARTIN E · 2019 to 2022
$1.9M
Circadian Regulation of Myocardial Insulin SignalingR01HL123574 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YOUNG, MARTIN E · 2014 to 2017
$1.5M
Basic and Translational Science in Heart FailureT32HL129948 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YOUNG, MARTIN E · 2017 to 2021
$1.4M
A Novel Role for IGF-1 Receptor in Growth Hormone ActionR01DK107441 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI FRANK, STUART J · 2016 to 2019
$1.3M
NHLBI NIH HHS R01 HL123574NHLBI NIH HHS R01 HL142216NHLBI NIH HHS R01 HL147549NHLBI NIH HHS R01 HL149159NHLBI NIH HHS T32 HL129948NIDDK NIH HHS R01 DK107441
6 · The paper itself

Abstract

Cell-autonomous circadian clocks have emerged as temporal orchestrators of numerous biological processes. For example, the cardiomyocyte circadian clock modulates transcription, translation, posttranslational modifications, ion homeostasis, signaling cascades, metabolism, and contractility of the heart over the course of the day. Circadian clocks are composed of more than 10 interconnected transcriptional modulators, all of which have the potential to influence the cardiac transcriptome (and ultimately cardiac processes). These transcriptional modulators include BMAL1 and REV-ERBα/β; BMAL1 induces REV-ERBα/β, which in turn feeds back to inhibit BMAL1. Previous studies indicate that cardiomyocyte-specific BMAL1-knockout (CBK) mice exhibit a dysfunctional circadian clock (including decreased REV-ERBα/β expression) in the heart associated with abnormalities in cardiac mitochondrial function, metabolism, signaling, and contractile function. Here, we hypothesized that decreased REV-ERBα/β activity is responsible for distinct phenotypical alterations observed in CBK hearts. To test this hypothesis, CBK (and littermate control) mice were administered with the selective REV-ERBα/β agonist SR-9009 (100 mg·kg

Indexed as

AnimalsARNTL Transcription FactorsCircadian ClocksCircadian RhythmGene ExpressionGene Expression RegulationHeartMiceMice, KnockoutMyocardiumMyocytes, CardiacNuclear Receptor Subfamily 1, Group D, Member 1PyrrolidinesThiophenesARNTL Transcription FactorsNr1d1 protein, mouseNuclear Receptor Subfamily 1, Group D, Member 1PyrrolidinesSR9009Thiopheneschronobiologygene expressionheartmetabolismmitochondria

Identifiers

PMID32357113
PMCPMC7311693
OpenAlexW3022481616

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.