Evidence map›Paper›PMID 40859366›Full record

ArticleStem cell research & therapy2025

Continuous adipose-derived stem cell therapy from the neonatal stage effectively reduces Duchenne muscular dystrophy symptoms in rats.

Yuki Kihara, Masanari Ikeda, Ryo Takagi, Keiko Ishigaki, Keitaro Yamanouchi, Satoru Nagata, Masayuki Yamato

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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.

Yuki KiharaDepartment of Pediatrics, School of Medicine, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan. kihara.yuki@twmu.ac.jp.ORCID http://orcid.org/0009-0003-9355-5397
Masanari IkedaDepartment of Veterinary Physiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, 113-8654, Japan.
Ryo TakagiInstitute of Advanced Biomedical Engineering and Science, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan.
Keiko IshigakiDepartment of Pediatrics, School of Medicine, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan.
Keitaro YamanouchiDepartment of Veterinary Physiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, 113-8654, Japan.
Satoru NagataDepartment of Pediatrics, School of Medicine, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan.
Masayuki YamatoInstitute of Advanced Biomedical Engineering and Science, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan.

Funding

Ministry of Education, Culture, Sports, Science and Technology JP23K14993Ministry of Health, Labour and Welfare 24FC1009Tokyo Women's Medical University Tokyo Women's Medical University
6 · The paper itself

Abstract

backgroundThe optimal timing for mesenchymal stem cell (MSC) therapy in Duchenne muscular dystrophy (DMD) remains unclear.

methodsNeonatal DMD rats received intraperitoneal adipose-derived MSCs according to three schedules: early (postnatal days 1 and 14), continuous (days 1, 14, 28, and 42), or late (days 28 and 42). Wild-type rats and untreated DMD rats served as controls. Functional and histological outcomes were assessed on day 56.

resultsContinuous administration significantly attenuated the decline in grip strength across ten consecutive measurements (- 11% vs. -37% in DMD controls), and also reduced serum creatine kinase levels and diaphragmatic fibrosis (p < 0.05). Early or late treatment alone showed limited benefit. GFP-labelled cells were rarely detected in muscle, indicating minimal engraftment and suggesting paracrine-mediated effects. Molecular profiling showed lower CDKN2A together with higher CDKN1A, IL-10, VEGF-A and IGF-1 in the continuous group, revealing an anti-senescence, pro-regenerative profile that paralleled the functional gains.

conclusionEarly and sustained MSC administration offers superior structural and functional protection in DMD rats, highlighting the importance of treatment timing in maximizing therapeutic efficacy.

Indexed as

Adipose TissueMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMuscular Dystrophy, DuchenneAnimalsAnimals, NewbornCreatine KinaseInsulin-Like Growth Factor IInterleukin-10MaleMuscle, SkeletalRatsVascular Endothelial Growth Factor ACreatine KinaseInsulin-Like Growth Factor IInterleukin-10Vascular Endothelial Growth Factor ACell therapyCellular senescenceDuchenne muscular dystrophyFibrosis SuppressionMesenchymal stem cells

Identifiers

PMID40859366
PMCPMC12382225

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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.