ArticleScientific reports2021
A 3D primary human cell-based in vitro model of non-alcoholic steatohepatitis for efficacy testing of clinical drug candidates.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 46 citations in OpenAlex.
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- Free Fatty acid-induced disruption of hepatic vitamin D metabolism impairs bone homeostasis in an in vitro 3D human liver-bone model.Archives of toxicology · 2026Article
- 3D Liver Fibrosis Models in Lab: A Novel Modality for Drug Screening.Pharmacology research & perspectives · 2026Review
- Reductive death is averted by a conserved de novo lipogenic switch.Molecular cell · 2026Article
- Glimpse into the role of Kupffer cells in a spheroid model of metabolic dysfunction-associated steatohepatitis (MASH).Biology open · 2026Article
- Integrating CRISPR genome editing with liver organoid and hiPSC-derived microfluidic platforms to model metabolic dysfunction-associated steatotic liver disease.Biochemistry and biophysics reports · 2026Review
- Human 3D liver spheroids support productive infection of a novel tick-borne phenuivirus.One health (Amsterdam, Netherlands) · 2026Article
- Hepatocyte Models for Metabolic Dysfunction-Associated Steatotic Liver Disease: A Comparative Analysis of Non-HepG2 Cell Models.International journal of molecular sciences · 2026Review
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- Excessive CabioRxiv : the preprint server for biology · 2026Article
- A microphysiological model of human MASLD reveals paradoxical response to resmetirom.Communications biology · 2026Article
- Scaling human liver microphysiological systems: implementing a higher-throughput liver acinus microphysiological system platform.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Primary Human Tissue Models for Metabolic Dysfunction-Associated Liver Disease - toward Streamlining Drug Discovery with Patient-Derived Assays.Advanced biology · 2025Review
- Microphysiological systems as an emerging in vitro approach for the evaluation of drug absorption, distribution, metabolism, and excretion and toxicity.Drug metabolism and disposition: the biological fate of chemicals · 2025Review
- Advanced 3D In Vitro Liver Fibrosis Models: Spheroids, Organoids, and Liver-on-Chips.Biomimetics (Basel, Switzerland) · 2025Review
- Development of anFrontiers in pharmacology · 2025Article
- Chemogenomic Screening in a Patient-Derived 3D Fatty Liver Disease Model Reveals the CHRM1-TRPM8 Axis as a Novel Module for Targeted Intervention.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Three-Dimensional Dynamic Cell Models for Metabolic Dysfunction-Associated Steatotic Liver Disease Progression.BME frontiers · 2025Article
- Organoids for Obesity-related Diseases: Disease Models and Drug Screening.Current stem cell research & therapy · 2025Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic steatohepatitis (NASH) is a progressive and severe liver disease, characterized by lipid accumulation, inflammation, and downstream fibrosis. Despite its increasing prevalence, there is no approved treatment yet available for patients. This has been at least partially due to the lack of predictive preclinical models for studying this complex disease. Here, we present a 3D in vitro microtissue model that uses spheroidal, scaffold free co-culture of primary human hepatocytes, Kupffer cells, liver endothelial cells and hepatic stellate cells. Upon exposure to defined and clinically relevant lipotoxic and inflammatory stimuli, these microtissues develop key pathophysiological features of NASH within 10 days, including an increase of intracellular triglyceride content and lipids, and release of pro-inflammatory cytokines. Furthermore, fibrosis was evident through release of procollagen type I, and increased deposition of extracellular collagen fibers. Whole transcriptome analysis revealed changes in the regulation of pathways associated with NASH, such as lipid metabolism, inflammation and collagen processing. Importantly, treatment with anti-NASH drug candidates (Selonsertib and Firsocostat) decreased the measured specific disease parameter, in accordance with clinical observations. These drug treatments also significantly changed the gene expression patterns of the microtissues, thus providing mechanisms of action and revealing therapeutic potential. In summary, this human NASH model represents a promising drug discovery tool for understanding the underlying complex mechanisms in NASH, evaluating efficacy of anti-NASH drug candidates and identifying new approaches for therapeutic interventions.
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