Evidence map›Paper›PMID 42477849›Full record

ArticleStem cell research & therapy2026

Miro1-mediated mitochondrial transfer boosts stem cell therapy for muscle atrophy via restoring mitochondrial homeostasis.

Fangling Zhao, Jingxin Fu, Linli Gao, Mengting Zhou, Yuhui Xia, Zexian Zhao, MengNa Yang, Jiahui He, Wei Zhu, Mengxiong Pan and 1 more

Abstract read
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In one paragraph

Article in Stem cell research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Fangling Zhao *Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No.88 Jiefang Road, Hangzhou, Zhejiang, China.
Jingxin Fu *Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No.88 Jiefang Road, Hangzhou, Zhejiang, China.
Linli Gao *Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No.88 Jiefang Road, Hangzhou, Zhejiang, China.
Mengting ZhouDepartment of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No.88 Jiefang Road, Hangzhou, Zhejiang, China.
Yuhui XiaDepartment of Neurology, Hangzhou Normal University Affiliated Hospital, Hangzhou, Zhejiang, China.
Zexian ZhaoDepartment of Neurology, Zhejiang Hospital, Zhejiang University School of Medicine, No.1229 Gudun Road, Hangzhou, China.
MengNa YangCollege of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Jiahui HeDepartment of Neurology, Hangzhou Hospital of Traditional Chinese Medicine, Zhejiang Chinese Medicine University, No.453 Tiyuchang Road, Hangzhou, Zhejiang, China.
Wei ZhuDepartment of Cardiology, Provincial Key Lab of Cardiovascular Research, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Mengxiong PanDepartment of Neurology, The First People's Hospital of Huzhou, First Affiliated Hospital of Huzhou University, Huzhou, China. panmx9182@163.com.
Kaiming LiuDepartment of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, No.88 Jiefang Road, Hangzhou, Zhejiang, China. Kaiming_liu@zju.edu.cn.

Funding

National Natural Science Foundation of China 82171561
6 · The paper itself

Abstract

Mitochondrial dysfunction underlies the major defect in muscle atrophy (characterized by the loss of skeletal muscle mass and function). Mesenchymal stem cells (MSCs), which can mediate mitochondrial transfer (MT) via tunneling nanotubes (TNTs), have been shown to exert therapeutic effects, yet the underlying mechanism remains unclear. Mitochondrial Rho GTPase 1 (Miro1) is crucial for regulating mitochondrial homeostasis; in this study, we aimed to investigate the roles of Miro1 and Milton in MSC-based therapy for muscle atrophy. Dexamethasone (DEX)-induced C2C12 cells and chronically aged mice were used as in vitro cellular and in vivo muscle atrophy models, respectively. In vitro experiments demonstrated that overexpression of Milton alone failed to enhance MT in DEX-induced C2C12 cells. Although Milton could promote the formation of TNTs, it was unable to drive mitochondrial movement along microtubules in the absence of Miro1.In contrast, Miro1 knockdown (MSCmiro1

Indexed as

Mesenchymal Stem CellsMitochondriaMitochondrial ProteinsMuscular Atrophyrho GTP-Binding ProteinsStem Cell TransplantationAnimalsCell LineDexamethasoneHomeostasisHumansMaleMiceMice, Inbred C57BLMuscle ProteinsMuscle, SkeletalDexamethasoneMitochondrial ProteinsMuscle Proteinsrho GTP-Binding ProteinsTrim63 protein, mouseTripartite Motif ProteinsUbiquitin-Protein LigasesMiro1Mitochondrial homeostasisMitochondrial transferMuscle atrophyStem cells

Identifiers

PMID42477849
PMCPMC13670476

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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.