Evidence map›Paper›PMID 39343927›Full record

ArticleSignal transduction and targeted therapy2024

Histone deacetylase inhibition enhances extracellular vesicles from muscle to promote osteogenesis via miR-873-3p.

Ming Chen, Yi Li, Mingming Zhang, Siliang Ge, Taojin Feng, Ruijing Chen, Junmin Shen, Ran Li, Zhongqi Wang, Yong Xie and 14 more

Abstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Review
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  3. Epigenetic Connections in Malocclusion.International journal of molecular sciences · 2026
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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

24 authors.

Ming Chen *Senior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Yi Li *Senior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Mingming Zhang *Senior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.ORCID 0000-0003-4677-5664
Siliang GeSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Taojin FengSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Ruijing ChenSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Junmin ShenSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Ran LiSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Zhongqi WangSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Yong XieSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Duanyang WangThe Department of Orthopedic Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Jiang LiuThe Department of Orthopedic Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Yuan LinThe Department of Orthopedic Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Feifan ChangSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Junyu ChenSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Xinyu SunSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Dongliang ChengSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Xiang HuangSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Fanfeng WuSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Qinxiang ZhangSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Pingqiang CaiJiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, China.ORCID 0000-0002-2665-5932
Pengbin YinSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China. yinpengbin@gmail.com.
Licheng ZhangSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China. zhanglcheng218@126.com.
Peifu TangSenior Department of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81972115National Natural Science Foundation of China (National Science Foundation of China) 82002330National Natural Science Foundation of China (National Science Foundation of China) 82202728
6 · The paper itself

Abstract

Regular physical activity is widely recognized for reducing the risk of various disorders, with skeletal muscles playing a key role by releasing biomolecules that benefit multiple organs and tissues. However, many individuals, particularly the elderly and those with clinical conditions, are unable to engage in physical exercise, necessitating alternative strategies to stimulate muscle cells to secrete beneficial biomolecules. Histone acetylation and deacetylation significantly influence exercise-induced gene expression, suggesting that targeting histone deacetylases (HDACs) could mimic some exercise responses. In this study, we explored the effects of the HDAC inhibitor Trichostatin A (TSA) on human skeletal muscle myoblasts (HSMMs). Our findings showed that TSA-induced hyperacetylation enhanced myotube fusion and increased the secretion of extracellular vesicles (EVs) enriched with miR-873-3p. These TSA-EVs promoted osteogenic differentiation in human bone marrow mesenchymal stem cells (hBMSCs) by targeting H2 calponin (CNN2). In vivo, systemic administration of TSA-EVs to osteoporosis mice resulted in significant improvements in bone mass. Moreover, TSA-EVs mimicked the osteogenic benefits of exercise-induced EVs, suggesting that HDAC inhibition can replicate exercise-induced bone health benefits. These results demonstrate the potential of TSA-induced muscle-derived EVs as a therapeutic strategy to enhance bone formation and prevent osteoporosis, particularly for individuals unable to exercise. Given the FDA-approved status of various HDAC inhibitors, this approach holds significant promise for rapid clinical translation in osteoporosis treatment.

Indexed as

Extracellular VesiclesHistone Deacetylase InhibitorsHydroxamic AcidsMicroRNAsOsteogenesisAnimalsCell DifferentiationHumansMesenchymal Stem CellsMiceMuscle, SkeletalOsteoporosisHistone Deacetylase InhibitorsHydroxamic AcidsMicroRNAstrichostatin A

Identifiers

PMID39343927
PMCPMC11439940

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.