Evidence map›Paper›PMID 41803645›Full record

ArticleStem cells (Dayton, Ohio)2026

Prostaglandin E2 receptor EP2 is indispensable for maintenance of skeletal muscle stem cells.

Yusuke Maruyama, Ken'ichiro Nogami, Norio Motohashi, Fusako Sakai-Takemura, Ahmed Elhussieny, Fumiaki Uchiumi, Yoshitsugu Aoki, Shin'ichi Takeda, Yuko Miyagoe-Suzuki

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cells (Dayton, Ohio), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

9 authors.

Yusuke MaruyamaDepartment of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, 187-8502, Japan.
Ken'ichiro NogamiDepartment of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, 187-8502, Japan.
Norio MotohashiDepartment of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, 187-8502, Japan.
Fusako Sakai-TakemuraDepartment of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, 187-8502, Japan.
Ahmed ElhussienyDepartment of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, 187-8502, Japan.
Fumiaki UchiumiDepartment of Gene Regulation, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Chiba, 278-8510, Japan.
Yoshitsugu AokiDepartment of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, 187-8502, Japan.
Shin'ichi TakedaDepartment of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, 187-8502, Japan.
Yuko Miyagoe-SuzukiDepartment of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, 187-8502, Japan.ORCID 0000-0001-8458-6237

Funding

Japan Agency for Medical Research and Development 19bm0804005h0103
6 · The paper itself

Abstract

Muscle satellite cells are adult muscle stem cells indispensable for growth and regeneration of postnatal skeletal muscle. Notch plays a central role in maintenance of muscle satellite cells, but how Notch maintains the muscle stem cell pool is not fully understood. Previously, we reported that a prostaglandin E2 receptor, EP2, is upregulated by Notch signal and suppresses differentiation of human muscle progenitors. Here we examined the roles of EP2 in muscle satellite cells using a mouse Cre-LoxP conditional gene knockout system. Genetic inactivation of the EP2 gene (PTGER2) activated muscle satellite cells, caused their loss, and impaired muscle regeneration. These results indicate that EP2 is indispensable for maintenance of satellite cells. Ex vivo analysis using isolated myofibers showed that prostaglandin E2 (PGE2) delayed the activation of satellite cells via EP2. An extracellular signal-regulated kinase (ERK) 1/2 inhibitor blocked the activation of satellite cells on myofibers, and PGE2 attenuated the phosphorylation of ERK1/2 in muscle satellite cells. These results suggest that EP2 keeps the quiescence of satellite cells and maintains the satellite cell pool in part by inhibiting the ERK1/2 signaling pathway.

Indexed as

Muscle, SkeletalReceptors, Prostaglandin E, EP2 SubtypeSatellite Cells, Skeletal MuscleStem CellsAnimalsCell DifferentiationDinoprostoneMiceMice, KnockoutDinoprostonePtger2 protein, mouseReceptors, Prostaglandin E, EP2 SubtypeEP2ERK1/2prostaglandin E2quiescenceskeletal muscle stem cells

Identifiers

PMID41803645
PMCPMC13110117

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.