ReviewThe FEBS journal2022
Liver macrophages and inflammation in physiology and physiopathology of non-alcoholic fatty liver disease.
Review in The FEBS journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 83 citations in OpenAlex.
- Cannabinoid 2 Receptor Activation Mitigates High-Fat Diet/Streptozotocin-Induced Nonalcoholic Fatty Liver Disease in Diabetic Mice by Modulation of Oxidative Stress, Inflammation, and Fibrosis.ACS pharmacology & translational science · 2026Article
- Periodontitis aggravates high-fat diet-induced MASLD via gut microbiota dysbiosis and metabolic dysfunction in mice.Scientific reports · 2026Article
- Systems mapping of intra-donor, cross-tissue T cell clonal expansion and tissue adaptation in the gut-liver-blood axis.Cell reports · 2026Article
- [Characterization of liver macrophage subsets in different mouse models of metabolic associated steatohepatitis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Article
- Pre-Eclampsia-Induced Maternal Liver Dysfunction: Systematic Review, Meta-Analysis and Meta-Regression of Observation Studies.Life (Basel, Switzerland) · 2026Review
- Tofogliflozin attenuates liver steatosis and fibrosis in non-diabetic non-alcoholic steatohepatitis mice.BMC gastroenterology · 2026Article
- The Role of Kupffer Cells and Liver Macrophages in the Pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease.Biomedicines · 2026Review
- Weight Regain after Lifestyle Interventions is Associated with Higher Risk of Liver Inflammation: A Retrospective Observational Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Spatial immune dysregulation in MASLD: integration of lobular zoning, metabolism and immune function.Frontiers in immunology · 2026Review
- Review
- Toxins to treatments: Impact of environmental pollutants, gut microbiota, and natural compounds on non-alcoholic fatty liver disease progression.World journal of hepatology · 2025Review
- Liver stiffness measurements in patients with metabolic dysfunction-associated steatotic liver disease: Updates on the method effectiveness and perspectives.World journal of hepatology · 2025Review
- D-Xylose Ameliorates Non-Alcoholic Fatty Liver Disease by Targeting Macrophage-expressed LYZ Gene.Cell biochemistry and biophysics · 2025Article
- Exploring the hepatic-ophthalmic axis through immune modulation and cellular dynamics in diabetic retinopathy and non-alcoholic fatty liver disease.Human genomics · 2025Article
- Research Progress on Anti-Inflammatory Mechanism ofInternational journal of molecular sciences · 2025Review
- FermentedJournal of microbiology and biotechnology · 2025Article
- Analysis of Factors Related to Pulmonary Nodules in Patients With Fatty Liver: A Large-Scale Cohort Study Based on a Physical Examination Population.International journal of general medicine · 2025Article
- Unraveling the RKIP-YY1 axis: immune crosstalk in the pathogenesis of metabolic disorders.Frontiers in immunology · 2025Review
- Research Progress on the Role and Mechanism of Flavonoids in Improving Metabolic Associated Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Three-Dimensional Dynamic Cell Models for Metabolic Dysfunction-Associated Steatotic Liver Disease Progression.BME frontiers · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome, being a common comorbidity of type 2 diabetes and with important links to inflammation and insulin resistance. NAFLD represents a spectrum of liver conditions ranging from steatosis in the form of ectopic lipid storage, to inflammation and fibrosis in nonalcoholic steatohepatitis (NASH). Macrophages that populate the liver play important roles in maintaining liver homeostasis under normal physiology and in promoting inflammation and mediating fibrosis in the progression of NAFLD toward to NASH. Liver macrophages are a heterogenous group of innate immune cells, originating from the yolk sac or from circulating monocytes, that are required to maintain immune tolerance while being exposed portal and pancreatic blood flow rich in nutrients and hormones. Yet, liver macrophages retain a limited capacity to raise the alarm in response to danger signals. We now know that macrophages in the liver play both inflammatory and noninflammatory roles throughout the progression of NAFLD. Macrophage responses are mediated first at the level of cell surface receptors that integrate environmental stimuli, signals are transduced through multiple levels of regulation in the cell, and specific transcriptional programmes dictate effector functions. These effector functions play paramount roles in determining the course of disease in NAFLD and even more so in the progression towards NASH. The current review covers recent reports in the physiological and pathophysiological roles of liver macrophages in NAFLD. We emphasise the responses of liver macrophages to insulin resistance and the transcriptional machinery that dictates liver macrophage function.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.