ArticleInternational journal of molecular sciences2020
Prolonged Lipid Accumulation in Cultured Primary Human Hepatocytes Rather Leads to ER Stress than Oxidative Stress.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Inappropriate Diet Exacerbates Metabolic Dysfunction-Associated Steatotic Liver Disease via Abdominal Obesity.Nutrients · 2024Pooled it
- 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
- The gut-liver axis in animal diseases: roles, mechanisms, and veterinary clinical applications.Frontiers in veterinary science · 2026Review
- Metabolic dysfunction‑associated steatotic liver disease: Pathogenesis, model and treatment (Review).International journal of molecular medicine · 2025Review
- Human Hepatocytes in Experimental Steatosis: Influence of Donor Sex and Sex Hormones.Biomedicines · 2025Article
- Human-induced pluripotent stem cell-based hepatic modeling of lipid metabolism-associated TM6SF2-E167K variant.Hepatology (Baltimore, Md.) · 2025Article
- Association between Dietary Index for Gut Microbiota (DI-GM) and non-alcoholic fatty liver disease (NAFLD): Evidence from NHANES 1999-2018.Asia Pacific journal of clinical nutrition · 2025Observational
- Article
- Alisol B 23-Acetate Down-Regulated GRP94 to Restore Endoplasmic Reticulum Homeostasis on Non-Alcoholic Steatohepatitis.Food science & nutrition · 2025Article
- Hepatotoxicity of Nanoparticle-Based Anti-Cancer Drugs: Insights into Toxicity and Mitigation Strategies.International journal of nanomedicine · 2025Review
- Insights of gut-liver axis in hepatic diseases: Mechanisms, clinical implications, and therapeutic potentials.World journal of gastrointestinal pharmacology and therapeutics · 2024Review
- Proanthocyanidins-Based Synbiotics as a Novel Strategy for Nonalcoholic Fatty Liver Disease (NAFLD) Risk Reduction.Molecules (Basel, Switzerland) · 2024Review
- 6-Gingerol, a Bioactive Compound ofJournal of experimental pharmacology · 2024Article
- Persistent Lipid Accumulation Leads to Persistent Exacerbation of Endoplasmic Reticulum Stress and Inflammation in Progressive NASH via the IRE1α/TRAF2 Complex.Molecules (Basel, Switzerland) · 2023Article
- Article
- Impaired fatty acid metabolism perpetuates lipotoxicity along the transition to chronic kidney injury.JCI insight · 2022Article
- Lipotoxicity as a Barrier for T Cell-Based Therapies.Biomolecules · 2022Review
- Article
- Validated Growth Rate-Dependent Regulation of Lipid Metabolism inInternational journal of molecular sciences · 2022Article
- Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Overweight has become a major health care problem in Western societies and is accompanied by an increasing incidence and prevalence of non-alcoholic fatty liver disease (NAFLD). The progression from NAFLD to non-alcoholic steatohepatitis (NASH) marks a crucial tipping point in the progression of severe and irreversible liver diseases. This study aims to gain further insight into the molecular processes leading to the evolution from steatosis to steatohepatitis. Steatosis was induced in cultures of primary human hepatocytes by continuous five-day exposure to free fatty acids (FFAs). The kinetics of lipid accumulation, lipotoxicity, and oxidative stress were measured. Additionally, ER stress was evaluated by analyzing the protein expression profiles of its key players: PERK, IRE1a, and ATF6a. Our data revealed that hepatocytes are capable of storing enormous amounts of lipids without showing signs of lipotoxicity. Prolonged lipid accumulation did not create an imbalance in hepatocyte redox homeostasis or a reduction in antioxidative capacity. However, we observed an FFA-dependent increase in ER stress, revealing thresholds for triggering the activation of pathways associated with lipid stress, inhibition of protein translation, and apoptosis. Our study clearly showed that even severe lipid accumulation can be attenuated by cellular defenses, but regenerative capacities may be reduced.
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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 OpenQuestion graph.