ArticleBiomaterials research2025
Engineered Mesenchymal Stem Cell-Derived Small Extracellular Vesicles Mitigate Liver Fibrosis by Delivering USP10 to Reprogram Macrophage Phenotype.
Article in Biomaterials research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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.
Who cites it
7 citing papers in PubMed.
- USP10 deubiquitinase: Physiological function, diseases and therapeutic target (Review).International journal of molecular medicine · 2026Review
- Article
- Extracellular Vesicles in Liver Fibrosis: Pathogenic Messengers, Diagnostic Biomarkers, and Therapeutic Nanovectors.Pharmaceutics · 2026Review
- Review
- Tissue regeneration strategies based on mesenchymal stem cell-derived extracellular vesicles: from bench to bedside.Burns & trauma · 2026Review
- Mechanisms, efficacy, and future perspectives of cellular-based therapies for liver fibrosis/cirrhosis: focusing on mesenchymal stromal cells.Cell & bioscience · 2025Review
- Application of stem cells in the precise diagnosis and treatment of liver diseases.World journal of gastroenterology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The utilization of mesenchymal stem cells (MSCs) serves as an encouraging strategy for treating liver fibrosis. However, precise mechanisms are not completely understood. Recently, small extracellular vesicles (sEVs) have emerged as major paracrine effectors mediating the anti-fibrotic effects of MSCs. This study seeks to examine the healing properties of MSCs-sEVs on liver fibrosis and decipher the associated signaling pathways. Herein, MSCs substantially ameliorated carbon tetrachloride (CCL4)-induced liver inflammation and fibrosis in mice, with this effect predominantly attributed to their derived sEVs. Both in vivo and in vitro experiments verified that MSCs-sEVs skewed the phenotype of liver macrophages into an anti-fibrotic phenotype. Mass spectrometry analysis showed that ubiquitin-specific peptidase 10 (USP10) was significantly enriched in MSCs-sEVs, which was critical for protection against liver fibrosis. USP10 stabilizes Krüppel-like factor 4 (KLF4) via deubiquitination, participating in the modulation of macrophage phenotypes. Mechanistically, KLF4 reprograms macrophages to enhance their anti-inflammatory and repairing functions by modulating NF-κB/STAT6 signaling and regulating the transcription of MMP12. Finally, the exogenous incorporation of USP10 into MSCs-sEVs via genetic engineering further potentiated their antifibrotic effects. These findings deepen the knowledge regarding the cellular pathways through which MSCs ameliorate liver fibrosis, offering a theoretical basis for sEV-based therapeutic strategies.
Identifiers
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Registered trials
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.