Evidence map›Paper›PMID 39563244›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

BMSC-derived exosomes promote osteoporosis alleviation via M2 macrophage polarization.

Yanbin Zhang, Jing Bai, Bin Xiao, Chunyan Li

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
–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

43 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  13. FeBioengineering (Basel, Switzerland) · 2026
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  17. Identification of a Force-Induced Sox9Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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

4 authors.

Yanbin Zhang *Department of Spine Surgery, National Center for Orthopaedics, Capital Medical University Affiliated Beijing Jishuitan Hospital, Beijing, 100035, People's Republic of China.
Jing Bai *Department of Trauma and Joint, The Third Affiliated Hospital of Beijing University of Traditional Chinese Medicine, Beijing, 100029, People's Republic of China.
Bin XiaoDepartment of Spine Surgery, National Center for Orthopaedics, Capital Medical University Affiliated Beijing Jishuitan Hospital, Beijing, 100035, People's Republic of China.
Chunyan LiDepartment of Clinial Laboratory, Capital Medical University Affiliated Beijing Jishuitan Hospital, Xinjiekou No. 31 East Street, Xicheng District, Beijing, 100035, People's Republic of China. lichunyan@jst-hosp.com.cn.ORCID 0009-0003-5639-2541

Funding

supported by Beijing Jishuitan Hospital Nova Program XKXX202212
6 · The paper itself

Abstract

Osteoporosis is characterized by reduced bone mass due to imbalanced bone metabolism. Exosomes derived from bone mesenchymal stem cells (BMSCs) have been shown to play roles in various diseases. This study aimed to clarify the regulatory function and molecular mechanism of BMSCs-derived exosomes in osteogenic differentiation and their potential therapeutic effects on osteoporosis. Exosomes were extracted from BMSCs. Bone marrow-derived macrophages (BMDMs) were cultured and internalized with BMSCs-derived exosomes. Real-time quantitative PCR was used to detect the expression of macrophage surface markers and tripartite motif (TRIM) family genes. BMDMs were co-cultured with human osteoblasts to assess osteogenic differentiation. Western blot was performed to analyze the ubiquitination of triggering receptor expressed on myeloid cell 1 (TREM1) mediated by TRIM25. An ovariectomized mice model was established to evaluate the role of TRIM25 and exosomes in osteoporosis. Exosomes were successfully isolated from BMSCs. BMSCs-derived exosomes upregulated TRIM25 expression, promoting M2 macrophage polarization and osteogenic differentiation. TRIM25 facilitated the ubiquitination and degradation of TREM1. Overexpression of TREM1 reversed the enhanced M2 macrophage polarization and osteogenic differentiation caused by TRIM25 overexpression. TRIM25 enhanced the protective effect of BMSCs-derived exosomes against bone loss in mice. These findings suggested that BMSCs-derived exosomes promoted osteogenic differentiation by regulating M2 macrophage polarization through TRIM25-mediated ubiquitination and degradation of TREM1. This mechanism might provide a novel approach for treating osteoporosis.

Indexed as

Cell DifferentiationExosomesMacrophagesMesenchymal Stem CellsOsteogenesisOsteoporosisAnimalsCells, CulturedDisease Models, AnimalFemaleHumansMacrophage ActivationMiceTripartite Motif ProteinsUbiquitinationUbiquitin-Protein LigasesTripartite Motif ProteinsUbiquitin-Protein LigasesBone mesenchymal stem cellsExosomePolarizationTREM1TRIM25Ubiquitination

Identifiers

PMID39563244
PMCPMC11577737

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.