ArticleCancer cell international2024
Metabolomics reveals ascorbic acid inhibits ferroptosis in hepatocytes and boosts the effectiveness of anti-PD1 immunotherapy in hepatocellular carcinoma.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Metabolic heterogeneity, networks, and biomarkers of drug-induced liver injury.Journal of pharmaceutical analysis · 2026Article
- The Multilayered Landscape of Ferroptosis: Plasticity, Propagation, and Evolutionary Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Inhibition of ferroptosis improves developmental competence of vitrified-warmed oocytes.Frontiers in endocrinology · 2026Article
- Vitamin C as a Cardioprotective Agent Against Doxorubicin-Induced Cardiotoxicity.Journal of the American Heart Association · 2025Review
- Vitamin C Inhibits Scale Drop Disease Virus Infectivity by Targeting Nrf2 to Reduce Ferroptosis.Antioxidants (Basel, Switzerland) · 2025Article
- Hematological toxicity of [EJNMMI radiopharmacy and chemistry · 2025Article
- Microbial metabolite-driven immune reprogramming in tumor immunotherapy: mechanisms and therapeutic perspectives.Frontiers in immunology · 2025Review
- Mechanisms of Vitamins Inhibiting Ferroptosis.Antioxidants (Basel, Switzerland) · 2024Review
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Authors and funding
11 authors.
Funding
Abstract
backgroundImmunotherapy combined with molecular targeted therapy is increasingly popular in patients with advanced hepatocellular carcinoma (HCC). However, immune-related adverse events(irAEs) brought on by immunotherapy increase the likelihood of side effects, thus it is important to look into ways to address this issue.
methodsDifferent metabolite patterns were established by analyzing metabolomics data in liver tissue samples from 10 patients(divided into severe and mild liver injury) before and after immuno-targeted therapy. After establishing a subcutaneous tumor model of HCC, the mice were divided into PBS group, ascorbic acid(AA) group, and anti-PD1 + tyrosine kinase inhibitor (TKI) group, anti-PD1 + TKI + AA group. Liver tissue were stained with hematoxylin-eosin staining(HE) and the content of aspartate transaminase (AST) and alanine transaminase(ALT) in blood were determined. The mechanism was confirmed by western blotting, mass cytometry, and other techniques.
resultsThrough metabolomics analysis, AA was significantly reduced in the sample of patients with severe liver injury caused by immuno-targeted therapy compared to patients with mild liver injury. The addition of AA in vivo experiments demonstrated a reduction in liver injury in mice. In the liver tissues of the anti-PD1 + TKI + AA group, the protein expressions of SLC7A11,GPX4 and the level of glutathione(GSH) were found to be higher compared to the anti-PD1 + TKI group. Mass cytometry analysis revealed a significant increase in the CD11b
conclusionsAA could reduce liver injury by preventing hepatocyte SLC7A11/GPX4 ferroptosis and improve the immunotherapy effect of anti-PD1 by boosting CD11b
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