ArticleStem cell research & therapy2025
Human umbilical cord mesenchymal stem cells attenuate liver fibrosis in mice and inhibit hepatic stellate cell activation by secreting soluble factors.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Cell Therapy in Advanced Cirrhosis: From Preclinical Evidence to Clinical Application.Gastro hep advances · 2026Review
- Long noncoding RNA X-inactive-specific transcript promotes hepatic fibrosis by suppressing ferroptosis in hepatic stellate cells via the miR-663a/GPX4 axis.Frontiers in physiology · 2025Article
- The CNTN1/Gilz pathway mediates the therapeutic effect of mesenchymal stem cells onCell transplantationArticle
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Authors and funding
9 authors.
Funding
Abstract
backgroundMesenchymal stem cells (MSCs) have emerged as promising candidates to treat clinical liver fibrosis. However, the key factors and mechanisms underlying their antifibrotic effects remain largely unclear. Our aims were to assess the therapeutic efficacy of human umbilical cord (UC) MSCs in a murine liver fibrosis model, and to dissect the influence of their secretome in vitro.
methodsLiver fibrosis was induced in mice using carbon tetrachloride (CCl₄). Fluorescent labeling was used to track UC-MSC distribution post-injection, comparing intraperitoneal (IP) and intravenous (IV) delivery. UC-MSCs were administered intraperitoneally weekly, starting at either fibrosis induction (prevention) or after six weeks (therapeutic). Fibrosis severity was evaluated by hematoxylin and eosin (H&E) staining, Masson's trichrome staining and immunohistochemical (IHC) staining for alpha smooth muscle actin (α-SMA). Human hepatic stellate LX-2 cells were treated with complete UC-MSC-conditioned medium (CM
resultsIP-injected UC-MSCs showed increased liver-specific accumulation compared to IV-injected UC-MSC that distributed mostly to the lungs. In vivo, IP-injected UC-MSC significantly reduced fibrosis, as evidenced by decreased histological damage, collagen deposition, and α-SMA expression. Both preventive and therapeutic UC-MSC IP-treatments were effective. In vitro, CM
conclusionsIP-administered therapeutic UC-MSCs preferentially accumulate in the liver and effectively prevent and reverse liver fibrosis in mice, while inhibiting hepatic stellate cell activation in vitro. The antifibrotic effects in vivo are likely primarily mediated by excreted soluble factors rather than extracellular vesicles.
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