Evidence map›Paper›PMID 41220805›Full record

ArticleFrontiers in bioengineering and biotechnology2025

Excessive DAO inhibits myoblast migration, leading to impaired myotube fusion and muscle strength decline by reducing ECM.

Xiang Liu, Jianchao Xue, Yiming Liang, Zhenggang Li, Rui Xu, Huaimei Yang, Yu Zhao, Qiyang Wang, Jianhong Hou, Sheng Lu

Abstract read
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In one paragraph

Article in Frontiers in bioengineering and biotechnology, 2025. 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. Frontiers in pharmacology · 2026
    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

10 authors.

Xiang Liu *Department of Orthopedics, The Key Laboratory of Digital Orthopaedics of Yunnan Province, The Clinical Medicine Center of Spinal and Spinal Cord Disorders of Yunnan Province, The First People's Hospital of Yunnan Province & The Affiliated Hospital of Kunming University of Science and Technology, Kunming, China.
Jianchao Xue *Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Yiming LiangDepartment of Orthopedics, The Key Laboratory of Digital Orthopaedics of Yunnan Province, The Clinical Medicine Center of Spinal and Spinal Cord Disorders of Yunnan Province, The First People's Hospital of Yunnan Province & The Affiliated Hospital of Kunming University of Science and Technology, Kunming, China.
Zhenggang LiDepartment of Orthopedics, The Key Laboratory of Digital Orthopaedics of Yunnan Province, The Clinical Medicine Center of Spinal and Spinal Cord Disorders of Yunnan Province, The First People's Hospital of Yunnan Province & The Affiliated Hospital of Kunming University of Science and Technology, Kunming, China.
Rui XuDepartment of Orthopedics, The Key Laboratory of Digital Orthopaedics of Yunnan Province, The Clinical Medicine Center of Spinal and Spinal Cord Disorders of Yunnan Province, The First People's Hospital of Yunnan Province & The Affiliated Hospital of Kunming University of Science and Technology, Kunming, China.
Huaimei YangDepartment of Orthopedics, The Key Laboratory of Digital Orthopaedics of Yunnan Province, The Clinical Medicine Center of Spinal and Spinal Cord Disorders of Yunnan Province, The First People's Hospital of Yunnan Province & The Affiliated Hospital of Kunming University of Science and Technology, Kunming, China.
Yu ZhaoDepartment of Orthopaedic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Qiyang WangDepartment of Orthopedics, The Key Laboratory of Digital Orthopaedics of Yunnan Province, The Clinical Medicine Center of Spinal and Spinal Cord Disorders of Yunnan Province, The First People's Hospital of Yunnan Province & The Affiliated Hospital of Kunming University of Science and Technology, Kunming, China.
Jianhong HouDepartment of Orthopedics, The Key Laboratory of Digital Orthopaedics of Yunnan Province, The Clinical Medicine Center of Spinal and Spinal Cord Disorders of Yunnan Province, The First People's Hospital of Yunnan Province & The Affiliated Hospital of Kunming University of Science and Technology, Kunming, China.
Sheng LuDepartment of Orthopedics, The Key Laboratory of Digital Orthopaedics of Yunnan Province, The Clinical Medicine Center of Spinal and Spinal Cord Disorders of Yunnan Province, The First People's Hospital of Yunnan Province & The Affiliated Hospital of Kunming University of Science and Technology, Kunming, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The molecular mechanisms underlying muscle strength decline, particularly in age-related conditions such as sarcopenia, remain poorly understood. Previous omics studies have suggested a potential association between AOC1 (encoding diamine oxidase, DAO, mainly expressed in intestine) and muscle weakness, but experimental validation and mechanistic insights are lacking. This study aims to investigate the influence of secretory DAO on muscle function and its potential receptors. Methods: Serum DAO levels were measured in elderly participants (n = 129) using ELISA and correlated with grip strength. Animal models included naturally aging C57 mice, rapidly aging SAMP8 mice, and a glycerol-induced acute muscle injury model were established to verify the role and content of DAO under overall condition. Results: Elderly males with low grip strength exhibited significantly higher serum DAO levels, while no such correlation was observed in females. Aged and injured mouse models showed elevated DAO content in skeletal muscle, accompanied by fast-twitch fiber loss. In C2C12 cells, adding DAO recombinant protein inhibited myoblast migration and fusion without affecting viability. Mechanistically, DAO bound to Fbln1, suppressed FAK phosphorylation (Y576/Y577), and disrupted cytoskeletal remodeling. Discussion: This study provides experimental evidence that exssive DAO impairs muscle strength by inhibiting myoblast migration and fusion via the Fbln1/FAK pathway. The findings reveal a potential regulation between different organs and cells, and highlight a novel metabolic-biomechanical uncoupling mechanism linked by DAO in sarcopenia.

Indexed as

AOC1DAOFbln1/FAK pathwaymetabolic-biomechanical crosstalksarcopenia

Identifiers

PMID41220805
PMCPMC12598007

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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.