ReviewCurrent opinion in lipidology2018
Non-parenchymal hepatic cell lipotoxicity and the coordinated progression of non-alcoholic fatty liver disease and atherosclerosis.
Review in Current opinion in lipidology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- IL-10 attenuates metabolic dysfunction-associated steatotic liver disease via modulation of hepatic responses to lipotoxicity.JCI insight · 2026Article
- Exploring drug repurposing as a therapeutic strategy for non-alcoholic fatty liver disease (NAFLD): identification of potential targets and pathways.Gastroenterology and hepatology from bed to bench · 2025Article
- Diagnostic value of CT liver-to-spleen attenuation ratio in patients with non-alcoholic fatty liver disease and atherosclerotic plaque.Pakistan journal of medical sciences · 2024Article
- Relationship between albumin-corrected anion gap and non-alcoholic fatty liver disease varied in different waist circumference groups: a cross-sectional study.European journal of medical research · 2024Article
- Methyl Cinnamate (MC) Alleviates Free Fatty Acids (FFAs) Induced Lipid Accumulation Through the AMPK Pathway in HepG2 Cells.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Type 2 Diabetes Mellitus, Non-Alcoholic Fatty Liver Disease, and Metabolic Repercussions: The Vicious Cycle and Its Interplay with Inflammation.International journal of molecular sciences · 2023Review
- Non-Parenchymal Cells and the Extracellular Matrix in Hepatocellular Carcinoma in Non-Alcoholic Fatty Liver Disease.Cancers · 2023Review
- Activation of Kupffer cells in NAFLD and NASH: mechanisms and therapeutic interventions.Frontiers in cell and developmental biology · 2023Review
- NAFLD: Mechanisms, Treatments, and Biomarkers.Biomolecules · 2022Review
- NADPH Oxidases Connecting Fatty Liver Disease, Insulin Resistance and Type 2 Diabetes: Current Knowledge and Therapeutic Outlook.Antioxidants (Basel, Switzerland) · 2022Review
- Nonalcoholic Fatty Liver Disease.Handbook of experimental pharmacology · 2022Review
- Resident macrophages of the lung and liver: The guardians of our tissues.Frontiers in immunology · 2022Review
- Emerging Roles of Calcium Signaling in the Development of Non-Alcoholic Fatty Liver Disease.International journal of molecular sciences · 2021Review
- Microtechnology-basedAPL bioengineering · 2021Review
- Immunonano-Lipocarrier-Mediated Liver Sinusoidal Endothelial Cell-Specific RUNX1 Inhibition Impedes Immune Cell Infiltration and Hepatic Inflammation in Murine Model of NASH.International journal of molecular sciences · 2021Article
- Mushroom-Derived Medicine? Preclinical Studies Suggest Potential Benefits of Ergothioneine for Cardiometabolic Health.International journal of molecular sciences · 2021Review
- The Role and Mechanism of Oxidative Stress and Nuclear Receptors in the Development of NAFLD.Oxidative medicine and cellular longevity · 2021Review
- Hepatic Choline Transport Is Inhibited During Fatty Acid-Induced Lipotoxicity and Obesity.Hepatology communications · 2020Article
- Pemafibrate, a selective PPARα modulator, prevents non-alcoholic steatohepatitis development without reducing the hepatic triglyceride content.Scientific reports · 2020Article
- Adeno-Associated Virus Serotype 8-Mediated Genetic Labeling of Cholangiocytes in the Neonatal Murine Liver.Pharmaceutics · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purpose of reviewNon-alcoholic fatty liver disease (NAFLD) appears to be independently associated with the development of atherosclerosis. The biological mechanisms underlying this association are complex, and likely involve liver-resident cell types other than hepatocytes. Thus, we review recent evidence that non-parenchymal hepatic cell responses to lipid excess contribute to the pathogenesis of both NAFLD and atherosclerosis. RECENT
findingsSignificant independent associations between NAFLD and atherosclerosis have been identified through cross-sectional studies and meta-analyses. Mechanistic studies in cell cultures and in rodent models suggest that liver-resident macrophages, activated hepatic stellate cells (HSC) and liver sinusoidal endothelial cells (LSEC) mount lipotoxic responses under NAFLD conditions which can contribute to the progression of both NAFLD and atherosclerosis. SUMMARY: Non-parenchymal hepatic cell types exhibit some similarity in their responses to lipid excess, and in their pathogenic mechanisms, which likely contribute to the coordinated progression of NAFLD and atherosclerosis. In response to lipotoxic conditions, macrophages, Kupffer cells and HSC initiate robust inflammatory responses, whereas LSEC generate excess reactive oxygen species (ROS). The extent to which inflammatory cytokines and ROS produced by non-parenchymal cells contribute to the progression of both NAFLD and atherosclerosis warrants further investigation.
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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.