Evidence map›Paper›PMID 25194572›Full record

ArticleNature medicine2014

STAT3 signaling controls satellite cell expansion and skeletal muscle repair.

Matthew Timothy Tierney, Tufan Aydogdu, David Sala, Barbora Malecova, Sole Gatto, Pier Lorenzo Puri, Lucia Latella, Alessandra Sacco

Abstract read
In one paragraph

Article in Nature medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 257 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
257citing papers in PubMed, 1 pooled it
17.5field-weighted citation impact, top 1% 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

257 citing papers in PubMed, 1 synthesis or guideline pooled it, 386 citations in OpenAlex.

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197 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

8 authors at 2 institutions in 2 countries.

Matthew Timothy Tierney1] Graduate School of Biomedical Sciences, Sanford-Burnham Medical Research Institute, La Jolla, California, USA. [2].
Tufan Aydogdu1] Development, Aging and Regeneration Program (DARe), Sanford-Burnham Medical Research Institute, La Jolla, California, USA. [2] Life Sciences Solutions, Thermo Fisher Scientific, Carlsbad, California, USA. [3].
David SalaDevelopment, Aging and Regeneration Program (DARe), Sanford-Burnham Medical Research Institute, La Jolla, California, USA.
Barbora MalecovaDevelopment, Aging and Regeneration Program (DARe), Sanford-Burnham Medical Research Institute, La Jolla, California, USA.
Sole GattoDevelopment, Aging and Regeneration Program (DARe), Sanford-Burnham Medical Research Institute, La Jolla, California, USA.
Pier Lorenzo Puri1] Development, Aging and Regeneration Program (DARe), Sanford-Burnham Medical Research Institute, La Jolla, California, USA. [2] Epigenetics and Regenerative Medicine, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Fondazione Santa Lucia, Rome, Italy.
Lucia Latella1] Epigenetics and Regenerative Medicine, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Fondazione Santa Lucia, Rome, Italy. [2] Institute of Translational Pharmacology, National Research Council of Italy, Rome, Italy.
Alessandra SaccoDevelopment, Aging and Regeneration Program (DARe), Sanford-Burnham Medical Research Institute, La Jolla, California, USA.
Sanford Burnham Prebys Medical Discovery Institute · USIstituto di Farmacologia Traslazionale · IT

Funding

Pathogenic Alterations of the 3D Epigenetic Landscape in Dystrophin-Deficient Skeletal Muscles and Reversal by Dystrophin Re-ExpressionR01AR056712 · NIAMS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI Pier Lorenzo Puri · 2009 to 2026
$7.3M
Signal-dependent switch of SWI/SNF by miRNAs & control of muscle stem cell fateR01AR052779 · NIAMS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI PURI, PIER LORENZO · 2006 to 2015
$4.1M
San Diego Skeletal Muscle Research CenterP30AR061303 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LIEBER, RICHARD L. · 2011 to 2015
$3.3M
Role of STAT3 in muscle stem cell activationR01AR064873 · NIAMS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI SACCO, ALESSANDRA · 2014 to 2018
$2.1M
Role of STAT3 signaling in muscle stem cell activationR03AR063328 · NIAMS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI SACCO, ALESSANDRA · 2013 to 2015
$293k
Role of proteoglycan sulfation during muscle regeneration in dystrophic animalsF31AR065923 · NIAMS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI TIERNEY, MATTHEW · 2014 to 2016
$63k
NIAMS NIH HHS F31 AR065923NIAMS NIH HHS P30 AR061303NIAMS NIH HHS R01 AR052779NIAMS NIH HHS R01AR052779NIAMS NIH HHS R01 AR056712NIAMS NIH HHS R01AR056712NIAMS NIH HHS R01 AR064873NIAMS NIH HHS R03 AR063328Telethon GTB12001
6 · The paper itself

Abstract

The progressive loss of muscle regenerative capacity with age or disease results in part from a decline in the number and function of satellite cells, the direct cellular contributors to muscle repair. However, little is known about the molecular effectors underlying satellite cell impairment and depletion. Elevated levels of inflammatory cytokines, including interleukin-6 (IL-6), are associated with both age-related and muscle-wasting conditions. The levels of STAT3, a downstream effector of IL-6, are also elevated with muscle wasting, and STAT3 has been implicated in the regulation of self-renewal and stem cell fate in several tissues. Here we show that IL-6-activated Stat3 signaling regulates satellite cell behavior, promoting myogenic lineage progression through myogenic differentiation 1 (Myod1) regulation. Conditional ablation of Stat3 in Pax7-expressing satellite cells resulted in their increased expansion during regeneration, but compromised myogenic differentiation prevented the contribution of these cells to regenerating myofibers. In contrast, transient Stat3 inhibition promoted satellite cell expansion and enhanced tissue repair in both aged and dystrophic muscle. The effects of STAT3 inhibition on cell fate and proliferation were conserved in human myoblasts. The results of this study indicate that pharmacological manipulation of STAT3 activity can be used to counteract the functional exhaustion of satellite cells in pathological conditions, thereby maintaining the endogenous regenerative response and ameliorating muscle-wasting diseases.

Indexed as

AgingAnimalsCell ProliferationCells, CulturedHumansMaleMiceMice, Inbred C57BLMice, Inbred mdxMice, KnockoutMuscle DevelopmentMyoD ProteinPAX7 Transcription FactorRegenerationSatellite Cells, Skeletal MuscleSignal TransductionMyoD1 myogenic differentiation proteinMyoD ProteinPax7 protein, mousePAX7 Transcription FactorSTAT3 protein, humanStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID25194572
PMCPMC4332844
OpenAlexW2047018308

What OpenQuestion holds

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Registered trials

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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.