ReviewFrontiers in cell and developmental biology2023
Activation of Kupffer cells in NAFLD and NASH: mechanisms and therapeutic interventions.
Review in Frontiers in cell and developmental biology, 2023. 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.
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Who cites it
50 citing papers in PubMed, 65 citations in OpenAlex.
- The monoacylglycerol acyltransferase 2 inhibitor VB-85387 reduces MASLD.Journal of lipid research · 2026Article
- ZFP90 Serves as a Transcriptional Brake on NF-κB Signaling to Attenuate Diet-Induced MASLD Progression.Nutrients · 2026Article
- The microbiota-gut-brain axis: novel mechanisms and therapeutic frontiers in obesity and type 2 diabetes.NPJ biofilms and microbiomes · 2026Review
- When the Liver Flares: Inflammatory and Immunometabolic Mechanisms Driving the Transition from MASLD to MASH.Inflammation · 2026Review
- Mume Flos ameliorates MASLD-associated cognitive impairment by attenuating IL-17/NF-κB-mediated metabolic neuroinflammation.Metabolic brain disease · 2026Article
- Review
- [SingleZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Article
- Estrogen deprivation induces hepatic inflammation, Indoleamine-2,3-dioxygenase 1, tryptophan catabolism, and plasma cholesterol.Scientific reports · 2026Article
- GLP-1 RAs for Treating Metabolic Dysfunction-Associated Steatosis Liver Disease: From GLP-1 Discovery to FDA Approval: A Comprehensive Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Insulin resistance: mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Obesity, Metabolic Syndrome and MASLD in Children: Inflammation as the Missing Link-A Short Narrative Review.Life (Basel, Switzerland) · 2026Review
- Alpha-Lipoic Acid Reduces NLRP3/ASC Expression and IL-1β Release in Kupffer Cells and Improves Insulin Signaling in FL83B Hepatocytes Exposed to a Conditioned Medium.Food science & nutrition · 2026Article
- Insulin Resistance and Inflammation.International journal of molecular sciences · 2026Review
- The Role of Kupffer Cells and Liver Macrophages in the Pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease.Biomedicines · 2026Review
- Nanotherapeutic Strategies for MASLD: From Pathological Mechanisms to Targeted Delivery Systems.International journal of nanomedicine · 2026Review
- The liver-brain axis, from its function to preventive therapeutic strategies in diseases.Frontiers in endocrinology · 2026Review
- Vitamin D and the metabolic-associated steatotic liver disease-type 2 diabetes axis: a scoping-narrative review of global evidence and emerging perspectives for Sub-Saharan Africa.Frontiers in epidemiology · 2026Review
- The Role of Neutrophils in Non-Alcoholic Fatty Liver Disease: Mechanisms and Clinical Significance.Journal of inflammation research · 2026Review
- Rheumatoid Factor Beyond Rheumatoid Arthritis: A Potential Marker of Cardiometabolic and Hepatic Risk.Biologics : targets & therapy · 2026Review
- Chronic PET-Microplastic Exposure: Disruption of Gut-Liver Homeostasis and Risk of Hepatic Steatosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are emerging as the leading causes of liver disease worldwide. These conditions can lead to cirrhosis, liver cancer, liver failure, and other related ailments. At present, liver transplantation remains the sole treatment option for end-stage NASH, leading to a rapidly growing socioeconomic burden. Kupffer cells (KCs) are a dominant population of macrophages that reside in the liver, playing a crucial role in innate immunity. Their primary function includes phagocytosing exogenous substances, presenting antigens, and triggering immune responses. Moreover, they interact with other liver cells during the pathogenesis of NAFLD, and this crosstalk may either delay or exacerbate disease progression. Stimulation by endogenous signals triggers the activation of KCs, resulting in the expression of various inflammatory factors and chemokines, such as NLRP3, TNF-α, IL-1B, and IL-6, and contributing to the inflammatory cascade. In the past 5 years, significant advances have been made in understanding the biological properties and immune functions of KCs in NAFLD, including their interactions with tissue molecules, underlying molecular mechanisms, signaling pathways, and relevant therapeutic interventions. Having a comprehensive understanding of these mechanisms and characteristics can have enormous potential in guiding future strategies for the prevention and treatment of NAFLD.
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What OpenQuestion 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 OpenQuestion graph.