ArticleMolecular biomedicine2025
Epithelial membrane protein 1 drives hepatic stellate cell activation via the TLN1/FAK cascade in MASLD donor liver transplantation.
Article in Molecular biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- A tale of dual role: HECT‑type E3 ubiquitin ligase mechanisms in liver diseases (Review).International journal of molecular medicine · 2026Review
- Immune Determinants of MASLD Progression: From Immunometabolic Reprogramming to Fibrotic Transformation.Biology · 2026Review
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Authors and funding
15 authors.
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Abstract
The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) has significantly increased, prompting the increased use of steatotic donor livers in transplantation, contributing to a higher incidence and severity of ischemia-reperfusion injury (IRI), necessitating the development of targeted interventions for MASLD-related liver transplantation (MASLD-IRI). Here, we identified epithelial membrane protein 1 (EMP1) as a potential diagnostic and therapeutic target in MASLD-IRI using multi-omics analysis and mechanistic investigations in rodent models and cells, further validating our findings in human samples. Phenotypic observations revealed significant activation of hepatic stellate cells (HSCs) under MASLD-IRI conditions, leading to increased inflammatory liver injury, which correlated with significant upregulation of EMP1 in HSC. Mechanistically, EMP1 upregulation inhibited SMAD-specific E3 ubiquitin-protein ligase 1 (SMURF1)-mediated ubiquitination and degradation of talin1 (TLN1) by competing with SMURF1 for the TLN1 binding site. The subsequent accumulation of TLN1 further promoted phosphorylation of focal adhesion kinase (FAK), establishing a pro-inflammatory signaling axis-EMP1/TLN1/FAK-that amplified HSC activation and aggravated liver injury. Silencing EMP1 suppressed the TLN1/FAK post-translational modification cascade, thereby attenuating HSC activation and downstream inflammation. These findings highlight the potential of EMP1 as a biomarker to monitor the prognosis of MASLD transplantation, as well as a therapeutic target to improve prognosis.
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