ArticleNature communications2024
Induction of a distinct macrophage population and protection from lung injury and fibrosis by Notch2 blockade.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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
25 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Role of Monocytes in the Natural History of Idiopathic Pulmonary Fibrosis: A Systematic Literature Review.International journal of molecular sciences · 2025Pooled it
- The role of myeloid immune cells in lung epithelial repair.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Canonical Notch2 signaling regulates development and maintenance of iron-recycling macrophages and iron homeostasis.Nature communications · 2026Article
- Macrophage regulation of extracellular matrix remodeling in aging skeletal muscle.Ageing research reviews · 2026Review
- The impact of hypoxia and glycolysis on liver fibrosis.Journal of translational medicine · 2026Article
- Pollutant particles enhance house dust mite induced type 2 inflammation and the recruitment of monocyte derived Cd11cParticle and fibre toxicology · 2026Article
- A population-scale atlas of blood and tissue in lupus nephritis.bioRxiv : the preprint server for biology · 2026Article
- RIPK3 Orchestrates Scar-Associated Macrophage Dysfunction to Drive Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Airway injury induces alveolar epithelial responses mediated by macrophages.Cell reports · 2026Article
- Spatially resolved integrative analysis of transcriptomic and metabolomic changes in tissue injury studies.Nature communications · 2026Article
- Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition.Frontiers in immunology · 2026Review
- Immunometabolic control of macrophage plasticity in wound healing: mechanistic insights and therapeutic opportunities.Frontiers in immunology · 2026Review
- Recent understanding of immunometabolic remodeling in pulmonary macrophages: homeostasis, chronic respiratory diseases, and therapeutic targeting.Frontiers in pharmacology · 2026Review
- Single-Cell Insights Into Macrophage Subtypes in Pulmonary Infections.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Monocyte-Derived LGMNResearch (Washington, D.C.) · 2026Article
- Systematic monocyte subset analysis reveals differential contribution of Notch signaling components to monocyte heterogeneity.iScience · 2025Article
- Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- The Landscape of SPP1Immunology · 2025Review
- Functional diversity of disorder-specific macrophages involved in various diseases.Inflammation and regeneration · 2025Review
Corrections and comments
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Authors and funding
27 authors.
Funding
Abstract
Macrophages are pleiotropic and diverse cells that populate all tissues of the body. Besides tissue-specific resident macrophages such as alveolar macrophages, Kupffer cells, and microglia, multiple organs harbor at least two subtypes of other resident macrophages at steady state. During certain circumstances, like tissue insult, additional subtypes of macrophages are recruited to the tissue from the monocyte pool. Previously, a recruited macrophage population marked by expression of Spp1, Cd9, Gpnmb, Fabp5, and Trem2, has been described in several models of organ injury and cancer, and has been linked to fibrosis in mice and humans. Here, we show that Notch2 blockade, given systemically or locally, leads to an increase in this putative pro-fibrotic macrophage in the lung and that this macrophage state can only be adopted by monocytically derived cells and not resident alveolar macrophages. Using a bleomycin and COVID-19 model of lung injury and fibrosis, we find that the expansion of these macrophages before lung injury does not promote fibrosis but rather appears to ameliorate it. This suggests that these damage-associated macrophages are not, by themselves, drivers of fibrosis in the lung.
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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.