Evidence map›Paper›PMID 30072727›Full record

ArticleNature communications2018

JNK regulates muscle remodeling via myostatin/SMAD inhibition.

Sarah J Lessard, Tara L MacDonald, Prerana Pathak, Myoung Sook Han, Vernon G Coffey, Johann Edge, Donato A Rivas, Michael F Hirshman, Roger J Davis, Laurie J Goodyear

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

69 citing papers in PubMed, 120 citations in OpenAlex.

  1. Trial
  2. The effects of a caffeine containing pre-workout supplement on βEuropean journal of applied physiology · 2023
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9 more citing papers are in PubMed but not listed here.

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

10 authors at 7 institutions in 4 countries.

Sarah J LessardResearch Division, Joslin Diabetes Center, Boston, 02215, MA, USA. sarah.lessard@joslin.harvard.edu.
Tara L MacDonaldResearch Division, Joslin Diabetes Center, Boston, 02215, MA, USA.
Prerana PathakResearch Division, Joslin Diabetes Center, Boston, 02215, MA, USA.
Myoung Sook HanProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, 01605, MA, USA.
Vernon G CoffeyFaculty of Health Sciences and Medicine, Bond University, Gold Coast, 4226, QLD, Australia.ORCID http://orcid.org/0000-0001-6837-1906
Johann EdgeMassey University, Palmerston North, 4442, New Zealand.
Donato A RivasJean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, 02111, MA, USA.
Michael F HirshmanResearch Division, Joslin Diabetes Center, Boston, 02215, MA, USA.
Roger J DavisProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, 01605, MA, USA.ORCID http://orcid.org/0000-0002-0130-1652
Laurie J GoodyearResearch Division, Joslin Diabetes Center, Boston, 02215, MA, USA.
Brigham and Women's Hospital · USJoslin Diabetes Center · USBond University · AUHoward Hughes Medical Institute · USMassey University · NZTufts University · USUniversity of Massachusetts Chan Medical School · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI LAURIE J GOODYEAR · 1986 to 2026
$50.5M
Exercise Regulation of Glucose Homeostasis Administrative SupplementR01DK101043 · NIDDK · JOSLIN DIABETES CENTER · PI LAURIE J GOODYEAR · 2013 to 2026
$7.3M
Adipose Tissue Metabolic Stress ResponsesR01DK112698 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DAVIS, ROGER J. · 2017 to 2025
$4.4M
Metabolic Stress SignalingR01DK107220 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DAVIS, ROGER J. · 2016 to 2023
$3.6M
Role of MicroRNAs on Age and Contraction-induced Skeletal Muscle GrowthK01AG047247 · NIA · TUFTS UNIVERSITY BOSTON · PI RIVAS, DONATO A · 2015 to 2019
$488k
American Heart Association (American Heart Association, Inc.) 15SDG25560057NIA NIH HHS K01 AG047247NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R01 DK101043NIDDK NIH HHS R01 DK107220NIDDK NIH HHS R01 DK112698
6 · The paper itself

Abstract

Skeletal muscle has a remarkable plasticity to adapt and remodel in response to environmental cues, such as physical exercise. Endurance exercise stimulates improvements in muscle oxidative capacity, while resistance exercise induces muscle growth. Here we show that the c-Jun N-terminal kinase (JNK) is a molecular switch that when active, stimulates muscle fibers to grow, resulting in increased muscle mass. Conversely, when muscle JNK activation is suppressed, an alternative remodeling program is initiated, resulting in smaller, more oxidative muscle fibers, and enhanced aerobic fitness. When muscle is exposed to mechanical stress, JNK initiates muscle growth via phosphorylation of the transcription factor, SMAD2, at specific linker region residues leading to inhibition of the growth suppressor, myostatin. In human skeletal muscle, this JNK/SMAD signaling axis is activated by resistance exercise, but not endurance exercise. We conclude that JNK acts as a key mediator of muscle remodeling during exercise via regulation of myostatin/SMAD signaling.

Indexed as

AdultAnimalsCell NucleusEnzyme ActivationGene Expression RegulationHEK293 CellsHumansHypertrophyIntegrasesJNK Mitogen-Activated Protein KinasesMice, Inbred C57BLMice, KnockoutMuscle DevelopmentMusclesMuscle, SkeletalMyostatinCre recombinaseIntegrasesJNK Mitogen-Activated Protein KinasesMyostatinSmad Proteins

Identifiers

PMID30072727
PMCPMC6072737
OpenAlexW2884155806

What OpenQuestion holds

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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.