ArticleFrontiers in immunology2020
Trem-2 Promotes Emergence of Restorative Macrophages and Endothelial Cells During Recovery From Hepatic Tissue Damage.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 63 citations in OpenAlex.
- Metabolic drivers of MASLD and MASH: from hormonal imbalance to fibrosis.Diabetologia · 2026Review
- A human single-cell atlas identifies OLR1Nature genetics · 2026Article
- Macrophage efferocytosis promotes inflammation resolution and accelerates wound healing.Communications biology · 2026Review
- Dynamic regulation and targeted interventions of macrophages in ischemia-reperfusion injury.Journal of advanced research · 2026Review
- TREM2-expressing macrophages in liver diseases.Trends in endocrinology and metabolism: TEM · 2026Review
- Temporal single-cell sequencing analysis reveals that GPNMB-expressing macrophages potentiate muscle regeneration.Experimental & molecular medicine · 2025Article
- Multiple machine learning algorithms identify 13 types of cell death-critical genes in large and multiple non-alcoholic steatohepatitis cohorts.Lipids in health and disease · 2025Article
- Current Therapeutic Landscape for Metabolic Dysfunction-Associated Steatohepatitis.International journal of molecular sciences · 2025Review
- Resident synovial macrophages in synovial fluid: Implications for immunoregulation.Clinical immunology (Orlando, Fla.) · 2025Article
- Innate immune cells link dietary cues to normal and abnormal metabolic regulation.Nature immunology · 2025Review
- A multi-omics approach combining causal inference andFrontiers in immunology · 2025Article
- Epithelial barrier hypothesis in the context of nutrition, microbial dysbiosis, and immune dysregulation in metabolic dysfunction-associated steatotic liver.Frontiers in immunology · 2025Review
- TREM2Frontiers in immunology · 2025Review
- Article
- TREM2-mediated Macrophage Glycolysis Promotes Skin Wound Angiogenesis via the Akt/mTOR/HIF-1α Signaling Axis.Current medical science · 2024Article
- Biological and clinical role of TREM2 in liver diseases.Hepatology communications · 2024Review
- Article
- Lipid-associated macrophages' promotion of fibrosis resolution during MASH regression requires TREM2.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Resident Synovial Macrophages in Synovial Fluid: Implications for Immunoregulation in Infectious and Inflammatory Arthritis.bioRxiv : the preprint server for biology · 2024Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages are pivotal in mounting liver inflammatory and tissue repair responses upon hepatic injury, showing remarkable functional plasticity. The molecular mechanisms determining macrophage transition from inflammatory to restorative phenotypes in the damaged liver remain unclear. Using mouse models of acute (APAP) and chronic (CCl4) drug-induced hepatotoxic injury we show that the immune receptor Trem-2 controls phenotypic shifts of liver macrophages and impacts endothelial cell differentiation during tissue recovery. Trem-2 gene ablation led to a delayed re-population of Kupffer cells correlating with deterred resolution of hepatic damage following acute and chronic injury. During tissue recovery, we found that macrophages transitioning to Kupffer cells expressed high levels of Trem-2. Acquisition of the transition phenotype was associated with a unique transcriptomic profile denoting strong responsiveness to oxidative stress and downmodulation of the pro-inflammatory phenotype, which was not observed in absence of Trem-2. During tissue recovery, lack of Trem-2 favored accumulation of a liver-damage associated endothelial cell population (LDECs), whose transcriptional program was compatible with endothelial de-differentiation. Accordingly, LDECs precursor potential is supported by the downregulation of surface endothelial cell markers and by striking
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