Evidence map›Paper›PMID 32015229›Full record

ArticleThe Journal of clinical investigation2020

Annexin A1 drives macrophage skewing to accelerate muscle regeneration through AMPK activation.

Simon McArthur, Gaëtan Juban, Thomas Gobbetti, Thibaut Desgeorges, Marine Theret, Julien Gondin, Juliana E Toller-Kawahisa, Chris P Reutelingsperger, Bénédicte Chazaud, Mauro Perretti and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
9.8field-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

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 181 citations in OpenAlex.

  1. Pooled it
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  6. Macrophage Derived TGF-β Recruits BMSCs for Initiation of Bone Formation During Fracture Healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  11. A Novel Dysferlin-Binding Kinase CK2α Promotes Plasma Membrane Repair in Dysferlinopathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  12. Pro-resolving Annexin A1-derived peptide Ac2-26 reduces nociception and mitigates joint damage in experimental osteoarthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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44 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

11 authors at 3 institutions in 4 countries.

Simon McArthurInstitute of Dentistry and.
Gaëtan JubanUniversité Claude Bernard Lyon 1, CNRS UMR-5310, INSERM U-1217, Institut NeuroMyoGène, Lyon, France.
Thomas GobbettiWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Thibaut DesgeorgesUniversité Claude Bernard Lyon 1, CNRS UMR-5310, INSERM U-1217, Institut NeuroMyoGène, Lyon, France.
Marine TheretUniversité Claude Bernard Lyon 1, CNRS UMR-5310, INSERM U-1217, Institut NeuroMyoGène, Lyon, France.
Julien GondinUniversité Claude Bernard Lyon 1, CNRS UMR-5310, INSERM U-1217, Institut NeuroMyoGène, Lyon, France.
Juliana E Toller-KawahisaWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Chris P ReutelingspergerDepartment of Biochemistry and.
Bénédicte ChazaudUniversité Claude Bernard Lyon 1, CNRS UMR-5310, INSERM U-1217, Institut NeuroMyoGène, Lyon, France.
Mauro PerrettiWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Rémi MounierUniversité Claude Bernard Lyon 1, CNRS UMR-5310, INSERM U-1217, Institut NeuroMyoGène, Lyon, France.
Université Claude Bernard Lyon 1 · FRQueen Mary University of London · GBMaastricht University · NL

Funding

Wellcome TrustWellcome Trust 086867/Z/08/Z
6 · The paper itself

Abstract

Understanding the circuits that promote an efficient resolution of inflammation is crucial to deciphering the molecular and cellular processes required to promote tissue repair. Macrophages play a central role in the regulation of inflammation, resolution, and repair/regeneration. Using a model of skeletal muscle injury and repair, herein we identified annexin A1 (AnxA1) as the extracellular trigger of macrophage skewing toward a pro-reparative phenotype. Brought into the injured tissue initially by migrated neutrophils, and then overexpressed in infiltrating macrophages, AnxA1 activated FPR2/ALX receptors and the downstream AMPK signaling cascade, leading to macrophage skewing, dampening of inflammation, and regeneration of muscle fibers. Mice lacking AnxA1 in all cells or only in myeloid cells displayed a defect in this reparative process. In vitro experiments recapitulated these properties, with AMPK-null macrophages lacking AnxA1-mediated polarization. Collectively, these data identified the AnxA1/FPR2/AMPK axis as an important pathway in skeletal muscle injury regeneration.

Indexed as

Muscle, SkeletalRegenerationSignal TransductionAdaptor Proteins, Signal TransducingAMP-Activated Protein KinasesAnimalsAnnexin A1MiceMice, KnockoutReceptors, Formyl PeptideAdaptor Proteins, Signal TransducingAMP-Activated Protein KinasesAnnexin A1annexin A1, mouseformyl peptide receptor 2, mouseHSH2 protein, mouseReceptors, Formyl PeptideHomeostasisInflammationMacrophagesMuscle BiologyProtein kinases

Identifiers

PMID32015229
PMCPMC7269594
OpenAlexW3004663884

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.