ArticleScientific reports2023
A model of hepatic steatosis with declined viability and function in a liver-organ-on-a-chip.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
- 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
- Hepatocyte Models for Metabolic Dysfunction-Associated Steatotic Liver Disease: A Comparative Analysis of Non-HepG2 Cell Models.International journal of molecular sciences · 2026Review
- Toxicological evaluation of Lagerstroemia speciosa (L.) Martyn and Lagerstroemia tomentosa C.Presl extracts using a liver organ-on-a-chip system.Scientific reports · 2026Article
- The HepG2 Cell Line as a Model for Studying Metabolic Dysfunction-Associated Steatotic Liver Disease.International journal of molecular sciences · 2026Review
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- Therapeutic potential of TMSC-Exo for non-alcoholic fatty liver disease using the liver-on-a-chip model.Journal of translational internal medicine · 2026Article
- Comparative study of palmitoleic acid, sea buckthorn oil, and lovastatin in hepatocellular steatosis model.Scientific reports · 2026Article
- Bridging the Gap Between Static Histology and Dynamic Organ-on-a-Chip Models.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Hongjam, an edible silkworm-derived food, attenuates steatohepatitis and fibrosis via multi-axis modulation of metabolic stress, inflammation, and fibrogenic signaling.Frontiers in nutrition · 2026Article
- Organ-on-a-chip platforms for disease modeling and in vitro diagnostic applications.Frontiers in bioengineering and biotechnology · 2026Review
- Modeling cancer-microbiome interactions in vitro: A guide to co-culture platforms.International journal of cancer · 2025Review
- Elafibranor: A promising therapeutic approach for liver fibrosis and gut barrier dysfunction in alcohol-associated liver disease.World journal of gastroenterology · 2025Review
- Engineering liver disease models in vitro: emerging trends and innovations.eGastroenterology · 2025Review
- Three-Dimensional Dynamic Cell Models for Metabolic Dysfunction-Associated Steatotic Liver Disease Progression.BME frontiers · 2025Article
- CHIP ameliorates nonalcoholic fatty liver disease via promoting K63- and K27-linked STX17 ubiquitination to facilitate autophagosome-lysosome fusion.Nature communications · 2024Article
- Collagen I Increases Palmitate-Induced Lipotoxicity in HepG2 Cells via Integrin-Mediated Death.Biomolecules · 2024Article
- Adipocyte inflammation is the primary driver of hepatic insulin resistance in a human iPSC-based microphysiological system.Nature communications · 2024Article
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fatty liver disease (NAFLD) begins with benign steatosis caused by ectopic storage of triacylglycerols in the liver. Persistent steatosis, in combination with other genetic and environmental factors, leads to nonalcoholic steatohepatitis (NASH) characterized by functional impairment, inflammation, and fibrosis. However, it remains unclear how persistent steatosis directly contributes to the progression of NAFLD, which may represent a therapeutic target. The organ-on-a-chip (OOC) has emerged as a new culture platform to recapitulate human pathological conditions under which drug candidates can be screened. Here, we developed a simple OOC steatosis model using the Mimetas OrganoPlate with a human liver cell line, HepG2. Treating the HepG2 OOCs with fatty acid overload induced steatosis within 24 h. Moreover, persistent steatosis for 6 days impaired OOC viability and hepatic function, as measured by a WST-8 assay and albumin production, respectively. Lastly, the HepG2 OOCs were exposed to drugs being tested in clinical trials for NAFLD/NASH during the 6-day period. Pioglitazone improved the OOC viability while elafibranor reduced the steatosis in association with reduced viability and albumin production. In conclusion, we show that the HepG2 steatosis OOC model is a useful tool on which the efficacy and toxicity of various therapeutic candidates can be tested.
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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 OpenQuestion graph.