ArticleCell & bioscience2024
Med1 inhibits ferroptosis and alleviates liver injury in acute liver failure via Nrf2 activation.
Article in Cell & bioscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Artemisiae Argyi exosome-like nanovesicles alleviate ALF by reducing oxidative stress and inhibiting inflammation through the TLR4/NLRP3/Nrf2 axis.Chinese medicine · 2026Article
- Ferroptosis regulatory networks and precision interventions in autoimmune hepatitis: comparison with cholestatic diseases.Frontiers in immunology · 2026Review
- Alpinetin pretreatment prevents lipopolysaccharide/D-galactosamine-induced acute liver injury in mice by inhibiting ferroptosis via the Nrf2/SLC7A11/GPX4 pathway.Scientific reports · 2025Article
- The protective effects and mechanism of myricetin in liver diseases (Review).Molecular medicine reports · 2025Review
- Potential Biomarkers and Therapeutic Targets in Hepatitis B Virus-related Acute Liver Failure: Interplay of the Ferroptosis, Autophagy and Immune Responses.International journal of medical sciences · 2025Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundExtensive hepatocyte mortality and the absence of specific medical therapy significantly contribute to the unfavorable prognosis of acute liver failure (ALF). Ferroptosis is a crucial form of cell death involved in ALF. In this study, we aimed to determine the impact of Mediator complex subunit 1 (Med1) on ferroptosis and its potential hepatoprotective effects in ALF.
resultsMed1 expression is diminished in the liver of lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced ALF mice, as well as in hepatocytes damaged by H
conclusionOverall, our research findings indicate that Med1 suppresses ferroptosis and alleviates liver injury in LPS/D-GalN-induced ALF through the activation of Nrf2. These findings substantiate the therapeutic viability of targeting the Med1-Nrf2 axis as a means of treating individuals afflicted with ALF.
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Registered trials
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