ArticlePloS one2025
Human umbilical cord-derived mesenchymal stem cells alleviate autoimmune hepatitis by inhibiting hepatic ferroptosis.
Article in PloS one, 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.
- Mesenchymal Stem/Stromal Cells and Their Derived Extracellular Vesicles: a Promising Therapeutic Strategy for Autoimmune Hepatitis.Clinical reviews in allergy & immunology · 2026Review
- Adipose tissue-derived mesenchymal stem cells combined with prednisone synergistically ameliorate autoimmune hepatitis in mice.Stem cell research & therapy · 2026Article
- Ferroptosis regulatory networks and precision interventions in autoimmune hepatitis: comparison with cholestatic diseases.Frontiers in immunology · 2026Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAutoimmune hepatitis (AIH) is a liver disease marked by immune-mediated hepatocyte damage. Current treatments have variable patient responses and considerable side effects, highlighting the need for alternative therapies. Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) have shown therapeutic potential in liver diseases, but their mechanisms in AIH remain unclear.
methodsA Concanavalin A (ConA)-induced AIH-like mouse model was used to assess the therapeutic effects of hUC-MSCs. Survival, liver function-related serum marker expression, histopathology, and apoptosis were evaluated. Metabolomic profiling and ferroptosis-related markers were analyzed to uncover potential mechanisms.
resultsIn ConA-induced AIH-like mouse model challenged with a lethal dose of ConA, hUC-MSC treatment significantly ameliorated liver tissue damage and serum liver function parameters, alleviated hepatocyte apoptosis, and improved survival. Metabolomic and ontology analyses of mouse liver tissue samples revealed that hUC-MSCs treatment altered the levels of metabolites (Glu derivatives and peptides) functionally associated with ferroptosis-related pathways. hUC-MSCs partially reversed ConA-induced malondialdehyde (MDA), oxidized glutathione (GSSG), glutamate, and Fe2+, while restoring reduced glutathione (GSH). Expression of COX2 was downregulated, whereas key ferroptosis suppressors, SLC7A11, GPX4, and FTH1, were upregulated following hUC-MSC treatment.
conclusionsBased on the above evidence, we propose that hUC-MSCs may ameliorate ConA-induced liver injury in mice, potentially through modulation of ferroptosis-related pathways, and we support further investigation of hUC-MSCs as potential treatments for AIH. We believe that further in-depth studies are still needed to elaborate on the detailed regulatory mechanisms of MSCs on the ferroptosis pathway during the treatment of AIH.
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