ArticleMolecular and cellular biochemistry2025
Extracellular vesicles derived from bone marrow mesenchymal stem cells ameliorate liver fibrosis via micro-7045-5p.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Mechanisms, efficacy, and future perspectives of cellular-based therapies for liver fibrosis/cirrhosis: focusing on mesenchymal stromal cells.Cell & bioscience · 2025Review
- Human umbilical cord-derived mesenchymal stem cells ameliorate non-alcoholic fatty liver disease via activating TFEB-mediated autophagy in male mice.Stem cell research & therapy · 2025Article
- Extracellular vesicles from Yiguanjian-primed bone-marrow mesenchymal stem cells ameliorate chronic liver fibrosis via miR-7045-5p.Stem cell research & therapy · 2025Article
- The Role of Extracellular Vesicles in Musculoskeletal Diseases.Journal of extracellular vesicles · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
introductionLiver fibrosis is a crucial pathological factor in the persistence and progression of chronic liver disease. Increasing evidence has demonstrated the significant potential of extracellular vesicles (EVs) secreted by bone marrow mesenchymal stem cells (BMSCs) in the clinical treatment of liver fibrosis. This study aimed to mechanistically investigate the impact of BMSC-derived EVs (BMSC-EVs) containing miR-7045-5p on the autophagy of activated hepatic stellate cells (HSCs) during liver fibrosis.
methodBMSCs were isolated from the bilateral femurs and tibiae of mice. Their identity was confirmed via immunofluorescence staining for the BMSC marker CD44. EVs were harvested from BMSC culture medium at passages 3-5 and then DiR-labeled. Labeled BMSC-EVs were co-cultured with the HSC-T6 cell line to determine their uptake and sub-cellular localization in HSCs. Various methods, such as western blotting, qRT-PCR, and ELISA, were employed to assess the effects of BMSC-EVs on the fibrotic activation (marked by COL1-A1 and α-SMA expression) and autophagy (p62, Atg16L1, Beclin-1, and LC3 expression) of HSC-T6 cells. Additionally, the BMSC-EV-induced changes in autophagy-related signaling pathways (PI3K, AKT, and mTOR pathways) in these cells were evaluated. Finally, the gene-chip detection technology was utilized to predict the involvement of BMSC-EV-derived miRNAs (BMSC-EV-miRs) in the observed effects, with a focus on miR-7045-5p, and our findings were validated in HSCs transfected with a miR-7045-5p mimic.
resultThe gene-chip detection results indicated that miR-7045-5p was enriched in BMSC-EVs compared with BMSCs and targeted Akt. In the CCl
conclusionBMSC-EVs promote autophagy in HSC-T6 cells and alleviate liver fibrosis by inhibiting the PI3K/Akt/mTOR signaling pathway at least in part by delivering anti-fibrotic miRNAs, such as miR-7045-5p.
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