ArticleJCI insight2024
Gpnmb and Spp1 mark a conserved macrophage injury response masking fibrosis-specific programming in the lung.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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
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Who cites it
34 citing papers in PubMed.
- Antifibrotic monocyte activation by nanoparticles resolves murine pulmonary fibrosis.Biomaterials · 2026Article
- Non-Resolving Repair in Idiopathic Pulmonary Fibrosis: From Failed Cellular Transitions to Architectural Lock-In.International journal of molecular sciences · 2026Review
- Review
- GPNMB Is Strongly Expressed in Foreign Body Giant Cells in Human and Mouse Tissues.Annals of dermatology · 2026Article
- SPP1+ macrophages contribute to silica-induced pulmonary inflammation and fibrosis via the ERK/JNK signaling pathway.American journal of respiratory cell and molecular biology · 2026Article
- POSTN(+) fibroblasts and SPP1(+) macrophages in scar formation: A review of mechanisms and therapeutic targets (Review).Molecular medicine reports · 2026Review
- Spatially Distinct Macrophage Subsets Drive Myofibroblast Heterogeneity and Maladaptive Fibrosis in Lupus Nephritis.bioRxiv : the preprint server for biology · 2026Article
- Anti-VEGF vascular remodeling drives germinal center B cell-rich tertiary lymphoid structures during antibody-toxin and anti-CD40 combination therapy in glioblastoma.Research square · 2026Article
- Pollutant particles enhance house dust mite induced type 2 inflammation and the recruitment of monocyte derived Cd11cParticle and fibre toxicology · 2026Article
- Longitudinal Single-Cell RNA-seq Profiling of Lung Cell Phenotypes, Signaling, and Cross-talk During Fibrosis Resolution.bioRxiv : the preprint server for biology · 2026Article
- A population-scale atlas of blood and tissue in lupus nephritis.bioRxiv : the preprint server for biology · 2026Article
- Chemoradiation Reprograms Tumor Cells and the Immune Microenvironment in Cervical Cancer.Cancer research · 2026Article
- Chemokine-defined macrophage niches establish spatial organization of tumor immunity.Nature immunology · 2026Article
- Clonal Hematopoiesis Instructs Maladaptive Tissue Repair to Promote Fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Airway injury induces alveolar epithelial responses mediated by macrophages.Cell reports · 2026Article
- Regulatory network architecture constrains inflammatory responses in tissue-resident alveolar macrophages.bioRxiv : the preprint server for biology · 2026Article
- Monocyte-Derived LGMNResearch (Washington, D.C.) · 2026Article
- Macrophage plasticity and metabolic control in muscle repair and disease.Frontiers in immunology · 2026Review
- Macrophage Phenotypic Plasticity and Inflammatory Mechanisms in Hyperoxia-Induced Lung Injury.Journal of inflammation research · 2026Review
- From inflammatory activation to fibrotic remodeling: the central role of macrophage heterogeneity in frozen shoulder.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Macrophages are required for healthy repair of the lungs following injury, but they are also implicated in driving dysregulated repair with fibrosis. How these 2 distinct outcomes of lung injury are mediated by different macrophage subsets is unknown. To assess this, single-cell RNA-Seq was performed on lung macrophages isolated from mice treated with LPS or bleomycin. Macrophages were categorized based on anatomic location (airspace versus interstitium), developmental origin (embryonic versus recruited monocyte derived), time after inflammatory challenge, and injury model. Analysis of the integrated dataset revealed that macrophage subset clustering was driven by macrophage origin and tissue compartment rather than injury model. Gpnmb-expressing recruited macrophages that were enriched for genes typically associated with fibrosis were present in both injury models. Analogous GPNMB-expressing macrophages were identified in datasets from both fibrotic and nonfibrotic lung disease in humans. We conclude that this subset represents a conserved response to tissue injury and is not sufficient to drive fibrosis. Beyond this conserved response, we identified that recruited macrophages failed to gain resident-like programming during fibrotic repair. Overall, fibrotic versus nonfibrotic tissue repair is dictated by dynamic shifts in macrophage subset programming and persistence of recruited macrophages.
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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.