ArticlePloS one2013
TLR-2/TLR-4 TREM-1 signaling pathway is dispensable in inflammatory myeloid cells during sterile kidney injury.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
- 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
- Damage Associated Molecular Patterns (DAMPs) Mediate the Foreign Body Response to Poly(ethylene glycol) Diacrylate Hydrogels via Toll like Receptors.ACS biomaterials science & engineering · 2025Article
- Small molecules as ligands in the tuning of immune regulatory receptors.Frontiers in immunology · 2025Review
- Diagnostic and Predictive Values of Soluble Triggering Receptor Expressed on Myeloid Cells-1 in Sepsis: A Multi-Center Prospective Clinical Study.Journal of inflammation research · 2025Article
- Inhibiting triggering receptor expressed on myeloid cells 1 signaling to ameliorate skin fibrosis.JCI insight · 2024Article
- Cellular senescence in ischemia/reperfusion injury.Cell death discovery · 2022Review
- Sphingosine 1-phosphate signaling in perivascular cells enhances inflammation and fibrosis in the kidney.Science translational medicine · 2022Article
- Article
- Identification of Auxiliary Biomarkers and Description of the Immune Microenvironmental Characteristics in Duchenne Muscular Dystrophy by Bioinformatical Analysis and Experiment.Frontiers in neuroscience · 2022Article
- Extracellular CIRP induces acute kidney injury via endothelial TREM-1.Frontiers in physiology · 2022Article
- Article
- Early Inflammation in Muscular Dystrophy Differs between Limb and Respiratory Muscles and Increases with Dystrophic Severity.The American journal of pathology · 2021Article
- Skin Resident γδ T Cell Function and Regulation in Wound Repair.International journal of molecular sciences · 2020Review
- Rheumatoid arthritis synovial fibroblasts promote TREM-1 expression in monocytes via COX-2/PGEArthritis research & therapy · 2019Article
- Inhibition of Triggering Receptor Expressed on Myeloid Cells 1 Ameliorates Inflammation and Macrophage and Neutrophil Activation in Alcoholic Liver Disease in Mice.Hepatology communications · 2019Article
- The triggering receptor expressed by myeloid cells-1 activates TLR4-MyD88-NF-κB-dependent signaling to aggravate ventilation-induced lung inflammation and injury in mice.Cell and tissue research · 2018Article
- TREM-1; Is It a Pivotal Target for Cardiovascular Diseases?Journal of cardiovascular development and disease · 2018Review
- Myeloid differentiation primary response gene (MyD) 88 signalling is not essential for intestinal fibrosis development.Scientific reports · 2017Article
- Pericyte MyD88 and IRAK4 control inflammatory and fibrotic responses to tissue injury.The Journal of clinical investigation · 2017Article
- Effect of TREM-1 blockade and single nucleotide variants in experimental renal injury and kidney transplantation.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Inflammatory macrophages are abundant in kidney disease, stimulating repair, or driving chronic inflammation and fibrosis. Damage associated molecules (DAMPs), released from injured cells engage pattern recognition receptors (PRRs) on macrophages, contributing to activation. Understanding mechanisms of macrophage activation during kidney injury may lead to strategies to alleviate chronic disease. We identified Triggering-Receptor-in-Myeloid-cells (TREM)-1, a regulator of TLR signaling, as highly upregulated in kidney inflammatory macrophages and tested the roles of these receptors in macrophage activation and kidney disease. Kidney DAMPs activated macrophages in vitro, independently of TREM-1, but partially dependent on TLR-2/-4, MyD88. In two models of progressive interstitial kidney disease, TREM-1 blockade had no impact on disease or macrophage activation in vivo, but TLR-2/-4, or MyD88 deficiency was anti-inflammatory and anti-fibrotic. When MyD88 was mutated only in the myeloid lineage, however, there was no bearing on macrophage activation or disease progression. Instead, TLR-2/-4 or MyD88 deficiency reduced activation of mesenchyme lineage cells resulting in reduced inflammation and fibrosis, indicating that these pathways play dominant roles in activation of myofibroblasts but not macrophages. To conclude, TREM-1, TLR2/4 and MyD88 signaling pathways are redundant in myeloid cell activation in kidney injury, but the latter appear to regulate activation of mesenchymal cells.
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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.