Evidence map›Paper›PMID 25896247›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2015

Monocyte/Macrophage-derived IGF-1 Orchestrates Murine Skeletal Muscle Regeneration and Modulates Autocrine Polarization.

Joanne Tonkin, Lieve Temmerman, Robert D Sampson, Enrique Gallego-Colon, Laura Barberi, Daniel Bilbao, Michael D Schneider, Antonio Musarò, Nadia Rosenthal

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers.

0numbers the graph read from it
0cells of the map it votes in
200citing papers in PubMed
11.0field-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

200 citing papers in PubMed, 310 citations in OpenAlex.

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  19. Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026
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140 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 4 countries.

Joanne TonkinMouse Biology Unit, European Molecular Biology Laboratory (EMBL), Monterotondo, Rome, Italy; National Heart and Lung Institute, Imperial College London, London, UK. Electronic address: j.tonkin@imperial.ac.uk.
Lieve TemmermanMouse Biology Unit, European Molecular Biology Laboratory (EMBL), Monterotondo, Rome, Italy; Current address: Department of Pathology, Maastricht University (CARIM), Maastricht, The Netherlands.
Robert D SampsonNational Heart and Lung Institute, Imperial College London, London, UK.
Enrique Gallego-ColonNational Heart and Lung Institute, Imperial College London, London, UK.
Laura BarberiInstitute Pasteur Cenci-Bolognetti, DAHFMO-Unit of Histology and Medical Embryology, IIM, Sapienza University of Rome, Rome, Italy.
Daniel BilbaoMouse Biology Unit, European Molecular Biology Laboratory (EMBL), Monterotondo, Rome, Italy.
Michael D SchneiderNational Heart and Lung Institute, Imperial College London, London, UK.
Antonio MusaròInstitute Pasteur Cenci-Bolognetti, DAHFMO-Unit of Histology and Medical Embryology, IIM, Sapienza University of Rome, Rome, Italy.
Nadia RosenthalMouse Biology Unit, European Molecular Biology Laboratory (EMBL), Monterotondo, Rome, Italy; National Heart and Lung Institute, Imperial College London, London, UK; Australian Regenerative Medicine Institute/EMBL Australia, Monash University, Melbourne, Australia.
Imperial College London · GBSapienza University of Rome · ITEuropean Molecular Biology Laboratory · ITMaastricht University · NLMonash University · AU

Funding

Medical Research Council G0901467Telethon GGP13013
6 · The paper itself

Abstract

Insulin-like growth factor 1 (IGF-1) is a potent enhancer of tissue regeneration, and its overexpression in muscle injury leads to hastened resolution of the inflammatory phase. Here, we show that monocytes/macrophages constitute an important initial source of IGF-1 in muscle injury, as conditional deletion of the IGF-1 gene specifically in mouse myeloid cells (ϕIGF-1 CKO) blocked the normal surge of local IGF-1 in damaged muscle and significantly compromised regeneration. In injured muscle, Ly6C+ monocytes/macrophages and CD206+ macrophages expressed equivalent IGF-1 levels, which were transiently upregulated during transition from the inflammation to repair. In injured ϕIGF-1 CKO mouse muscle, accumulation of CD206+ macrophages was impaired, while an increase in Ly6C+ monocytes/macrophages was favored. Transcriptional profiling uncovered inflammatory skewing in ϕIGF-1 CKO macrophages, which failed to fully induce a reparative gene program in vitro or in vivo, revealing a novel autocrine role for IGF-1 in modulating murine macrophage phenotypes. These data establish local macrophage-derived IGF-1 as a key factor in inflammation resolution and macrophage polarization during muscle regeneration.

Indexed as

Wound HealingAnimalsAutocrine CommunicationGene Expression Regulation, DevelopmentalInflammationInsulin-Like Growth Factor IMacrophagesMiceMonocytesMuscle, SkeletalRegenerationinsulin-like growth factor-1, mouseInsulin-Like Growth Factor I

Identifiers

PMID25896247
PMCPMC4817788
OpenAlexW1979173328

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.