ArticleInternational journal of hepatology2024
Acyl-CoA Thioesterase 1 Contributes to Transition of Steatosis to Metabolic-Associated Steatohepatitis.
Article in International journal of hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02148471 (Non-alcoholic Steatohepatitis Versus Simple Hepatic Steatosis), which is not on this map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Non-alcoholic Steatohepatitis Versus Simple Hepatic Steatosis: Is There a Difference in the Nutritional Factors Influencing Lipid Perioxidation and Inflammation?
Who cites it
4 citing papers in PubMed.
- ACOT1-specific expression modulates metabolic reprogramming in diabetic cardiomyopathy: The role of SREBP1c lactylation in CD36-mediated lipotoxicity.American heart journal plus : cardiology research and practice · 2026Article
- Dietary α-Tocopherol Deficiency Disrupts Hepatic Circadian Clock and Lipid Metabolism in Association with Gut Microbiota Dysbiosis.Nutrients · 2026Article
- Orphan drug uttroside B impedes MASH progression and HCC development in experimental models.JHEP reports : innovation in hepatology · 2026Article
- Genome-Wide Association Study and RNA-Seq Analysis Uncover Candidate Genes Controlling Growth Traits in Red Tilapia (International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Metabolic dysfunction-associated steatohepatitis (MASH) has become the leading cause of chronic liver disease, but there has been no approved pharmacotherapy to date. Methods: We used a network analysis approach to delineate protein-protein interactions that contribute to the transition from steatosis to MASH, in order to identify and target this transition as a potential pharmacotherapeutic strategy. Acyl-CoA thioesterase 1 (ACOT1) was identified as a critical node in the protein-protein interaction (PPI) network of the transition from steatosis to MASH in patient samples. ACOT1 overexpression and silencing effects were tested Results: ACOT1 expression was 3-fold higher in MASH as compared to steatosis. In patient samples, Conclusion: These results suggest that ACOT1 contributes to the transition from steatosis to MASH through modulation of glycerophospholipid accumulation and its potential as a novel therapeutic target in MASH. This trial is registered with NCT02148471.
Identifiers
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Registered trials
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