Evidence map›Paper›PMID 30872796›Full record

ArticleScientific reports2019

The Nuclear Receptor and Clock Repressor Rev-erbα Suppresses Myogenesis.

Somik Chatterjee, Hongshan Yin, Weini Li, Jeongkyung Lee, Vijay K Yechoor, Ke Ma

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 52 citations in OpenAlex.

  1. New insights into the skeletal muscle circadian clock in ruminants.Journal of animal science and biotechnology · 2026
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  11. Effect ofFrontiers in veterinary science · 2024
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  15. Molecular clocks, satellite cells, and skeletal muscle regeneration.American journal of physiology. Cell physiology · 2023
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Somik ChatterjeeCenter for Diabetes Research, Department of Medicine, Houston Methodist Research Institute, Houston, TX, 77030, USA.
Hongshan YinCenter for Diabetes Research, Department of Medicine, Houston Methodist Research Institute, Houston, TX, 77030, USA.
Weini LiDepartment of Diabetes Complications & Metabolism, Beckman Research Institute of City of Hope, Duarte, CA, 91010, USA.
Jeongkyung LeeDiabetes and Beta Cell Biology Center, Division of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, 15213, USA.
Vijay K YechoorDiabetes and Beta Cell Biology Center, Division of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, 15213, USA.
Ke MaDepartment of Diabetes Complications & Metabolism, Beckman Research Institute of City of Hope, Duarte, CA, 91010, USA. kema@coh.org.
Beckman Research InstituteUniversity of Pittsburgh · USHouston Methodist · USThird Hospital of Hebei Medical University · CN

Funding

Transgenic Mouse FacilityP30CA033572 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI STANLEY R. HAMILTON · 1985 to 2026
$86.3M
Circadian Clock Control of Adipose Depot Development and FunctionR01DK112794 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI MA, KE · 2018 to 2021
$1.7M
Circadian Clock and Beta Cell Stress AdaptationR01DK097160 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI YECHOOR, VIJAY K · 2014 to 2018
$1.7M
NCI NIH HHS P30 CA033572NIDDK NIH HHS R01 DK097160NIDDK NIH HHS R01 DK112794
6 · The paper itself

Abstract

Rev-erbα is a ligand-dependent nuclear receptor and a key repressor of the molecular clock transcription network. Accumulating evidence indicate that the circadian clock machinery governs diverse biological processes in skeletal muscle, including muscle growth, repair and mass maintenance. The physiological function of Rev-erbα in myogenic regulation remains largely unknown. Here we show that Rev-erbα exerts cell-autonomous inhibitory effects on proliferation and differentiation of myogenic precursor cells, and these actions concertedly inhibit muscle regeneration in vivo. Mechanistic studies reveal Rev-erbα direct transcriptional control of two major myogenic mechanisms, proliferative pathway and the Wnt signaling cascade. Consistent with this finding, primary myoblasts lacking Rev-erbα display significantly enhanced proliferative growth and myogenic progression. Furthermore, pharmacological activation of Rev-erbα activity attenuates, whereas its inhibition by an antagonist promotes these processes. Notably, upon muscle injury, the loss-of-function of Rev-erbα in vivo augmented satellite cell proliferative expansion and regenerative progression during regeneration. Collectively, our study identifies Rev-erbα as a novel inhibitory regulator of myogenic progenitor cell properties that suppresses postnatal myogenesis. Pharmacological interventions to dampen Rev-erbα activity may have potential utilities to enhance regenerative capacity in muscle diseases.

Indexed as

Gene Expression RegulationAnimalsBiomarkersCell DifferentiationCell ProliferationCLOCK ProteinsDisease SusceptibilityGene Expression ProfilingMiceMice, KnockoutMuscle DevelopmentMuscle, SkeletalMyoblastsNuclear Receptor Subfamily 1, Group D, Member 1Orphan Nuclear ReceptorsRegenerationBiomarkersCLOCK ProteinsNuclear Receptor Subfamily 1, Group D, Member 1Orphan Nuclear Receptors

Identifiers

PMID30872796
PMCPMC6418265
OpenAlexW2921993406

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.