Evidence map›Paper›PMID 28607093›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Prostaglandin E2 is essential for efficacious skeletal muscle stem-cell function, augmenting regeneration and strength.

Andrew T V Ho, Adelaida R Palla, Matthew R Blake, Nora D Yucel, Yu Xin Wang, Klas E G Magnusson, Colin A Holbrook, Peggy E Kraft, Scott L Delp, Helen M Blau

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

156 citing papers in PubMed, 225 citations in OpenAlex.

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  10. 15-PGDH inhibition promotes muscle repair and strength recovery during GLP-1 receptor agonist-induced weight loss.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  14. Molecular evolution of animal aging.The EMBO journal · 2026
    Review
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96 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 3 institutions in 2 countries.

Andrew T V HoBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA 94305-5175.
Adelaida R PallaBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA 94305-5175.
Matthew R BlakeBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA 94305-5175.
Nora D YucelBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA 94305-5175.
Yu Xin WangBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA 94305-5175.
Klas E G MagnussonBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA 94305-5175.
Colin A HolbrookBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA 94305-5175.
Peggy E KraftBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA 94305-5175.
Scott L DelpDepartment of Bioengineering, Stanford University School of Medicine, Stanford, CA 94305.
Helen M BlauBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA 94305-5175; hblau@stanford.edu.
Baxter (United States) · USKTH Royal Institute of Technology · SEStanford University · US

Funding

Translational Oncology Research Program (Project-005)P30CA124435 · NCI · STANFORD UNIVERSITY · PI Melinda L. Telli · 2007 to 2026
$71.4M
GENETICS TRAINING PROGRAM FOR PHD CANDIDATEST32GM007790 · NIGMS · STANFORD UNIVERSITY · PI BRUNET, ANNE, KINGSLEY, DAVID M · 1985 to 2020
$12.8M
Stem Cells for Brain and BrawnR01AG020961 · NIA · STANFORD UNIVERSITY · PI BLAU, HELEN M · 2002 to 2019
$5.0M
Telomere extension using nucleoside-modified mRNA and exosomes as a novel therapeR01AR063963 · NIAMS · STANFORD UNIVERSITY · PI BLAU, HELEN M · 2012 to 2016
$4.3M
Mass Cytometry Analysis of Signaling Dysfunction in Duchenne Muscular DystrophyR01NS089533 · NINDS · STANFORD UNIVERSITY · PI BLAU, HELEN M · 2014 to 2017
$1.3M
NCI NIH HHS P30 CA124435NIAMS NIH HHS R01 AR063963NIA NIH HHS R01 AG020961NIGMS NIH HHS T32 GM007790NINDS NIH HHS R01 NS089533
6 · The paper itself

Abstract

Skeletal muscles harbor quiescent muscle-specific stem cells (MuSCs) capable of tissue regeneration throughout life. Muscle injury precipitates a complex inflammatory response in which a multiplicity of cell types, cytokines, and growth factors participate. Here we show that Prostaglandin E2 (PGE2) is an inflammatory cytokine that directly targets MuSCs via the EP4 receptor, leading to MuSC expansion. An acute treatment with PGE2 suffices to robustly augment muscle regeneration by either endogenous or transplanted MuSCs. Loss of PGE2 signaling by specific genetic ablation of the EP4 receptor in MuSCs impairs regeneration, leading to decreased muscle force. Inhibition of PGE2 production through nonsteroidal anti-inflammatory drug (NSAID) administration just after injury similarly hinders regeneration and compromises muscle strength. Mechanistically, the PGE2 EP4 interaction causes MuSC expansion by triggering a cAMP/phosphoCREB pathway that activates the proliferation-inducing transcription factor,

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalCyclic AMPCyclic AMP Response Element-Binding ProteinDinoprostoneMiceMuscle, SkeletalMyoblasts, SkeletalNuclear Receptor Subfamily 4, Group A, Member 2Receptors, Prostaglandin E, EP4 SubtypeRegenerationSignal TransductionAnti-Inflammatory Agents, Non-SteroidalCreb1 protein, mouseCyclic AMPCyclic AMP Response Element-Binding ProteinDinoprostoneNr4a2 protein, mouseNuclear Receptor Subfamily 4, Group A, Member 2Ptger4 protein, mouseReceptors, Prostaglandin E, EP4 Subtypemuscle stem cellsNSAIDsPGE2regenerationstrength

Identifiers

PMID28607093
PMCPMC5495271
OpenAlexW2624934173

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.