ArticleJournal of translational medicine2018
CCL20 is up-regulated in non-alcoholic fatty liver disease fibrosis and is produced by hepatic stellate cells in response to fatty acid loading.
Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 73 citations in OpenAlex.
- Serum CC-Chemokine Profiling in Alcohol-Associated Liver Disease: Focus on MIP-3α/CCL20 as a Biomarker of Disease Severity.Diagnostics (Basel, Switzerland) · 2026Article
- Chemokines and chemokine receptors in metabolic dysfunction-associated steatohepatitis: pathogenic mechanisms and clinical implications.Cellular & molecular biology letters · 2026Review
- CCL20-CCR6 axis mediates mucosal-associated invariant T-M2 macrophage crosstalk to drive immune dysregulation in liver cirrhosis.Frontiers in immunology · 2026Article
- Nidogen 1-enriched extracellular vesicles promote liver metastasis by inducing EMT and activating stellate cells.iScience · 2025Article
- Association Between Serum HBV DNA Levels and CCL-20, CD8a, CXCL-16, and GDF-15 in Patients with Chronic Hepatitis B.Viruses · 2025Article
- Myeloid cells in chronic liver inflammation.Cellular & molecular immunology · 2025Review
- The Intriguing Roles of Cytokines in Metabolic Dysfunction-Associated Steatotic Liver Disease: A Narrative Review.Current obesity reports · 2025Review
- Elevated CCL20 and IL-10 enhance 5-fluorouracil tolerance in colon cancer.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Novel predictors of preeclampsia and pregnancy complications: the impact of type 1 diabetes mellitus on maternal and fetal circulatory levels.Physiological research · 2025Article
- Identification of tryptophan metabolism-related biomarkers for nonalcoholic fatty liver disease through network analysis.Endocrine connections · 2025Article
- Colorectal cancer cells-derived exosomal miR-188-3p promotes liver metastasis by creating a pre-metastatic niche via activation of hepatic stellate cells.Journal of translational medicine · 2025Article
- Novel regulators of hepatic macrophages in liver fibrosis.Frontiers in immunology · 2025Review
- Identification of Diagnostic Biomarkers for Compensatory Liver Cirrhosis Based on Gut Microbiota and Urine Metabolomics Analyses.Molecular biotechnology · 2024Article
- Senescence-associated secretory phenotype (SASP) and uterine fibroids: Association with PD-L1 activation and collagen deposition.Ageing research reviews · 2024Review
- Article
- Crosstalk between purinergic receptor P2YCellular and molecular life sciences : CMLS · 2024Article
- Linking fatty liver diseases to hepatocellular carcinoma by hepatic stellate cells.Journal of the National Cancer Center · 2024Review
- Identification and validation of hub genes expressed in ulcerative colitis with metabolic dysfunction-associated steatotic liver disease.Frontiers in immunology · 2024Article
- Unveiling the role of ferroptosis in the progression from NAFLD to NASH: recent advances in mechanistic understanding.Frontiers in endocrinology · 2024Review
- Molecular mechanisms and treatment responses of pulmonary fibrosis in severe COVID-19.Respiratory research · 2023Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundNonalcoholic fatty liver disease (NAFLD) is a prevalent complication of extreme obesity. Loading of the liver with fat can progress to inflammation and fibrosis including cirrhosis. The molecular factors involved in the progression from simple steatosis to fibrosis remain poorly understood.
methodsGene expression profiling using microarray, PCR array, and RNA sequencing was performed on RNA from liver biopsy tissue from patients with extreme obesity. Patients were grouped based on histological findings including normal liver histology with no steatosis, lobular inflammation, or fibrosis, and grades 1, 2, 3, and 4 fibrosis with coexistent steatosis and lobular inflammation. Validation of expression was conducted using quantitative PCR. Serum analysis was performed using ELISA. Expression analysis of hepatocytes and hepatic stellate cells in response to lipid loading were conducted in vitro using quantitative PCR and ELISA.
resultsThree orthogonal methods to profile human liver biopsy RNA each identified the chemokine CCL20 (CC chemokine ligand 20 or MIP-3 alpha) gene as one of the most up-regulated transcripts in NAFLD fibrosis relative to normal histology, validated in a replication group. CCL20 protein levels in serum measured in 224 NAFLD patients were increased in severe fibrosis (p < 0.001), with moderate correlation of hepatic transcript levels and serum levels. Expression of CCL20, but not its cognate receptor CC chemokine receptor 6, was significantly (p < 0.001) increased in response to fatty acid loading in LX-2 hepatic stellate cells, with relative increases greater than those in HepG2 hepatocyte cells.
conclusionsThese results suggest that expression of CCL20, an important inflammatory mediator, is increased in NAFLD fibrosis. CCL20 serves as a chemoattractant molecule for immature dendritic cells, which have been shown to produce many of the inflammatory molecules that mediate liver fibrosis. These data also point to hepatic stellate cells as a key cell type that may respond to lipid loading of the liver.
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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.