ArticleThe Journal of clinical investigation2018
The innate immune receptor TREM-1 promotes liver injury and fibrosis.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed.
- Exosomes target liver TREM-1 to break the systemic inflammatory cascade and improve spinal cord injury outcomes.Journal of orthopaedic translation · 2026Article
- Exercise reduces hepatic pre-metastatic niche formation via TREM-1 signaling in kupffer cells.BMC medicine · 2026Article
- TREM1-mediated macrophage activation drives voriconazole-induced hepatic steatosis: Diagnostic and therapeutic implications.Journal of pharmaceutical analysis · 2026Article
- Single-cell and spatial transcriptomics reveal Thbs1-CD36 crosstalk between Kupffer and hepatic stellate cells following mesenchymal stem cell-derived small extracellular vesicles transplantation, alleviating liver fibrosis.Journal of nanobiotechnology · 2026Article
- Paeoniflorin Modulates TREM-1/NF-κB/LXRα/ABCG1 Pathway to Improve Cholesterol Metabolism and Inflammation in Hyperlipidemic Rat.International journal of molecular sciences · 2026Article
- Article
- Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages.Frontiers in immunology · 2026Review
- Triggering Receptor Expressed on Myeloid Cells-1 (TREM-1) in Inflammation and Disease: Mechanisms, Therapeutic Potential, and Future Directions.International journal of molecular sciences · 2025Review
- Myeloid cells in chronic liver inflammation.Cellular & molecular immunology · 2025Review
- SUCNR1 Deficiency Alleviates Liver Ischemia-Reperfusion Injury by Regulating Kupffer Cell Activation and Polarization Through the ERK/NF-κB Pathway in Mice.Inflammation · 2025Article
- The role of liver macrophages in viral liver pathogenesis.Journal of leukocyte biology · 2025Review
- Myeloid-Derived Suppressor Cell Accumulation Drives Intestinal Fibrosis through mCCL6/hCCL15 Chemokine-Mediated Fibroblast Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Infiltrating peripheral monocyte TREM-1 mediates dopaminergic neuron injury in substantia nigra of Parkinson's disease model mice.Cell death & disease · 2025Article
- TREM-1 inhibitor specificity and timing of treatment initiation can impact its therapeutic efficacy in cancer and inflammatory disease.Frontiers in oncology · 2025Article
- A multi-omics approach combining causal inference andFrontiers in immunology · 2025Article
- Article
- TREM1 is essential for maintaining stemness of liver cancer stem-like cells in hepatocellular carcinoma.Frontiers in immunology · 2025Article
- The Effect of Curcumin on the Activity of MMP-17 and MMP-24 in Hepatocytes of Mice Exposed to Thioacetamide.Reports of biochemistry & molecular biology · 2024Article
- Hepatocyte-specific CCAAT/enhancer binding protein α restricts liver fibrosis progression.The Journal of clinical investigation · 2024Article
- TC14012 enhances the anti-fibrosis effects of UC-MSCs on the liver by reducing collagen accumulation and ameliorating inflammation.Stem cell research & therapy · 2024Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Inflammation occurs in all tissues in response to injury or stress and is the key process underlying hepatic fibrogenesis. Targeting chronic and uncontrolled inflammation is one strategy to prevent liver injury and fibrosis progression. Here, we demonstrate that triggering receptor expressed on myeloid cells 1 (TREM-1), an amplifier of inflammation, promotes liver disease by intensifying hepatic inflammation and fibrosis. In the liver, TREM-1 expression was limited to liver macrophages and monocytes and was highly upregulated on Kupffer cells, circulating monocytes, and monocyte-derived macrophages in a mouse model of chronic liver injury and fibrosis induced by carbon tetrachloride (CCl4) administration. TREM-1 signaling promoted proinflammatory cytokine production and mobilization of inflammatory cells to the site of injury. Deletion of Trem1 reduced liver injury, inflammatory cell infiltration, and fibrogenesis. Reconstitution of Trem1-deficient mice with Trem1-sufficient Kupffer cells restored the recruitment of inflammatory monocytes and the severity of liver injury. Markedly increased infiltration of liver fibrotic areas with TREM-1-positive Kupffer cells and monocytes/macrophages was found in patients with hepatic fibrosis. Our data support a role of TREM-1 in liver injury and hepatic fibrogenesis and suggest that TREM-1 is a master regulator of Kupffer cell activation, which escalates chronic liver inflammatory responses, activates hepatic stellate cells, and reveals a mechanism of promotion of liver fibrosis.
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