ReviewLaboratory animal research2018
The role of hepatic macrophages in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis.
Review in Laboratory animal research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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
46 citing papers in PubMed.
- Meta-inflammation through the lens of macrophage programming and nutrient-sensing ghrelin signaling.Immunometabolism (Cobham, Surrey) · 2026Review
- Review
- Aerobic Exercise Alleviates Oxidative Stress and Inflammation to Attenuate High-Fat Diet-Induced Non-Alcoholic Fatty Liver Disease inMetabolites · 2026Article
- Dehydrotrametenolic acid methyl ester, a triterpenoid of Poria cocos, alleviates non-alcoholic steatohepatitis by suppressing NLRP3 inflammasome activation via targeting Caspase-1 in mice.Acta pharmacologica Sinica · 2025Article
- MIST1 regulates endoplasmic reticulum stress-induced hepatic apoptosis as a candidate marker of fatty liver disease progression.Cell death & disease · 2024Article
- Novel Peripherally Selective Cannabinoid Receptor 1 Neutral Antagonist Improves Metabolic Dysfunction-Associated Steatotic Liver Disease in Mice.ACS pharmacology & translational science · 2024Article
- Proanthocyanidins-Based Synbiotics as a Novel Strategy for Nonalcoholic Fatty Liver Disease (NAFLD) Risk Reduction.Molecules (Basel, Switzerland) · 2024Review
- Metabolic Reprograming of Macrophages: A New Direction in Traditional Chinese Medicine for Treating Liver Failure.Journal of immunology research · 2024Review
- Article
- S100A6 Activates Kupffer Cells via the p-P38 and p-JNK Pathways to Induce Inflammation, Mononuclear/macrophage Infiltration Sterile Liver Injury in Mice.Inflammation · 2023Article
- Vsig4Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Non-Parenchymal Cells and the Extracellular Matrix in Hepatocellular Carcinoma in Non-Alcoholic Fatty Liver Disease.Cancers · 2023Review
- Cellular heterogeneity and plasticity during NAFLD progression.Frontiers in molecular biosciences · 2023Review
- Immunometabolism in type 2 diabetes mellitus: tissue-specific interactions.Archives of medical science : AMS · 2023Article
- Myeloid-specific blockade of Notch signaling ameliorates nonalcoholic fatty liver disease in mice.International journal of biological sciences · 2023Article
- Neutrophil extracellular traps enriched with IL-1β and IL-17A participate in the hepatic inflammatory process of patients with non-alcoholic steatohepatitis.Virchows Archiv : an international journal of pathology · 2022Article
- Improvement in insulin sensitivity and prevention of high fat diet-induced liver pathology using a CXCR2 antagonist.Cardiovascular diabetology · 2022Article
- High-fat diet-induced nonalcoholic steatohepatitis is accelerated by low carnitine and impaired glucose tolerance in novel murine models.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Mitochondria homeostasis: Biology and involvement in hepatic steatosis to NASH.Acta pharmacologica Sinica · 2022Article
- The Association of Sarcopenia and Visceral Obesity with Lean Nonalcoholic Fatty Liver Disease in Chinese Patients with Type 2 Diabetes Mellitus.Journal of diabetes research · 2022Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic steatohepatitis (NASH) is becoming common chronic liver disease because of the increasing global prevalence of obesity and consequently Nonalcoholic fatty liver disease (NAFLD). However, the mechanism for progression of NAFLD to NASH and then cirrhosis is not completely understood, yet. The triggering of these hepatic diseases is thought from hepatocyte injury caused by over-accumulated lipid toxicity. Injured hepatocytes release damage-associated molecular patterns (DAMPs), which can stimulate the Kupffer cells (KCs), liver-resident macrophages, to release pro-inflammatory cytokines and chemokines, and recruit monocyte-derived macrophages (MDMs). The increased activation of KCs and recruitment of MDMs accelerate the progression of NAFLD to NASH and cirrhosis. Therefore, characterization for activation of hepatic macrophages, both KCs and MDMs, is a baseline to figure out the progression of hepatic diseases. The purpose of this review is to discuss the current understanding of mechanisms of NAFLD and NASH, mainly focusing on characterization and function of hepatic macrophages and suggests the regulators of hepatic macrophages as the therapeutic target in hepatic diseases.
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