Evidence map›Paper›PMID 40245180›Full record

ArticleJournal of cellular and molecular medicine2025

Sphingosine-1-Phosphate Receptor 2 Agonist Mobilises Endogenous Muse Cells to Repair Damaged Myocardial Tissue in Male Rabbits.

Shingo Minatoguchi, Yoshihisa Yamada, Noriko Endo, Hiromitsu Kanamori, Atsushi Mikami, Hiroyuki Okura, Shinya Minatoguchi

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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

7 authors.

Shingo MinatoguchiDepartment of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan.
Yoshihisa YamadaDepartment of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan.
Noriko EndoDepartment of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan.
Hiromitsu KanamoriDepartment of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan.
Atsushi MikamiDepartment of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan.
Hiroyuki OkuraDepartment of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan.
Shinya MinatoguchiDepartment of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan.ORCID 0000-0002-8159-9697

Funding

Japan Agency for Medical Research and Development (AMED)Ministry of Education, Culture, Sports, Science, and Technology (MEXT) and JSPS KAKENHI JP18K15843
6 · The paper itself

Abstract

Muse cells, pluripotent stem cells present mainly in the bone marrow (BM) selectively accumulate to damaged tissue by sensing sphingosine-1-phosphate (S1P) and replace damaged cells by differentiating in situ. Acute myocardial infarction (AMI) model rabbits were subcutaneously injected either with Vehicle (n = 15), S1PR2-agonist (n = 16), or S1PR2-agonist + S1PR2-antagonist (n = 10). The number of Muse cells in the peripheral blood was assessed by flow cytometry at 12 h after AMI. The S1PR2-agonist group showed a significant increase in the peripheral-blood Muse cell number at 12 h (p < 0.05), as well as infarct size reduction (p < 0.05) and improvement of left ventricular (LV) function (p < 0.05) at 2 weeks compared with the other 2 groups. The number of peripheral-blood Muse cells positively correlated with LV ejection fraction (p < 0.05) and inversely correlated with infarct size (p < 0.05). Transplanted autologous green fluorescent protein (GFP)-labelled BM-Muse cells into the BM, followed by the administration of either Vehicle (n = 5) or S1PR2 agonist (n = 5) revealed a higher number of homed GFP-Muse cells expressing the cardiac markers troponin-I, α-actinin, connexin-43 and the vascular marker CD31 in the border areas in the S1PR2-agonist group compared with the vehicle group. The mobilisation of endogenous Muse cells using S1PR2-agonist may be a promising therapeutic approach.

Indexed as

Myocardial InfarctionMyocardiumReceptors, LysosphingolipidAnimalsBone Marrow CellsDisease Models, AnimalLysophospholipidsMaleRabbitsSphingosineSphingosine-1-Phosphate ReceptorsVentricular Function, LeftLysophospholipidsReceptors, LysosphingolipidSphingosinesphingosine 1-phosphateSphingosine-1-Phosphate Receptorscardiac functionendogenous muse cellsinfarct sizemobilisationmyocardial infarctionsphingosine‐1‐phosphate receptor 2 agonist

Identifiers

PMID40245180
PMCPMC12005397

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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.