ArticleFrontiers in pharmacology2025
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Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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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.
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Who cites it
1 citing paper in PubMed.
- Hepatocyte Models for Metabolic Dysfunction-Associated Steatotic Liver Disease: A Comparative Analysis of Non-HepG2 Cell Models.International journal of molecular sciences · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
Introduction: Metabolic dysfunction-associated steatotic liver disease (MASLD) is estimated to affect ∼30% of adults globally. The progressive form of MASLD, metabolic dysfunction-associated steatohepatitis (MASH), is a leading cause of chronic liver disease. MASH is marked by hepatocellular fat accumulation (steatosis), ballooning, and inflammation. Although many Methods: Lipid-cytokine treatments were first optimized using differentiated HuH-7 cells based on cellular toxicity and their ability to induce a MASH-like phenotype. Three final treatments-all including TNF-α (1 ng/mL) and IL-6 (1.2 ng/mL)-were selected for SCHH evaluation: (1) oleic acid (OA):palmitic acid (PA) (1:2, 0.5 mM), (2) a lipid mix (lysophospholipids mixture + OA:PA), and (3) lipid mix + 0.01 mM cholesterol. Treatments were incubated for 72 h with SCHH from three donors. Quantitative targeted absolute proteomics (QTAP) assessed the transporter and DME concentrations, whereas B-CLEAR Results: All three treatments significantly increased lipid droplet formation and peroxidation in SCHH with minimal toxicity. These treatments also altered DME and transporter concentrations in a manner similar to the changes observed in liver tissue from patients with MASH. Across treatments, concentrations of the bile salt export pump (BSEP), sodium taurocholate co-transporting polypeptide (NTCP), organic anion transporting polypeptide (OATP) 1B1, OATP1B3, and multidrug resistance-associated protein (MRP) 2 were reduced by 0.66-0.57-fold, 0.71-0.52-fold, 0.74-0.63-fold, 0.82-0.80-fold, and 0.71-0.48-fold, respectively. Correspondingly, the TCA apparent uptake clearance and biliary clearance were reduced by 0.70-0.26-fold and 0.61-0.27-fold, respectively. E Discussion: These findings demonstrate that lipid-cytokine treatments induce MASH-like changes in SCHH, including clinically relevant reductions in DME and transporter concentrations and function. This model may serve as a valuable tool for predicting altered hepatobiliary drug disposition in MASH.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.