ArticleScience (New York, N.Y.)2025
Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage.
Article in Science (New York, N.Y.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- The role of myeloid immune cells in lung epithelial repair.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Alveolar Macrophages: Development, Respiratory Homeostasis, Signal Pathways, Diseases, and Therapeutic Opportunities.MedComm · 2026Review
- Pathophysiological roles of monocytes and macrophages in cancer.Nature reviews. Immunology · 2026Review
- Intratumoral Mycobacterium abscessus promotes cytidine deaminase mutagenesis in non-small cell lung cancer.Signal transduction and targeted therapy · 2026Article
- Targeting the immune-metabolic axis reverses orthodontics-induced systemic pathology.Signal transduction and targeted therapy · 2026Article
- Ocular IL-1α/IFN-γ Delay the Corneal Wound Healing in Rheumatoid Arthritis Through Mitochondrial Dysfunction and NLRP3 Inflammasome Activation.Investigative ophthalmology & visual science · 2026Article
- Metabolically engineered probiotic OMVs as nanovaccine mediating sequential immunomodulation for chronic bone infection immunotherapy.Cell reports. Medicine · 2026Article
- Article
- Influenza A/PR8 virus infection in mice suppresses basal and Oncostatin M-induced IL-33 expression in vivo and in vitro.Scientific reports · 2026Article
- Spatially Distinct Macrophage Subsets Drive Myofibroblast Heterogeneity and Maladaptive Fibrosis in Lupus Nephritis.bioRxiv : the preprint server for biology · 2026Article
- Clinical significance of miR-548a-3p and its potential role in acute respiratory distress syndrome complicated with pulmonary fibrosis via OSM.BMC immunology · 2026Article
- The 2025 lung cancer landscape: advances in screening, molecular taxonomy and therapeutic strategy: a narrative review.Translational lung cancer research · 2026Review
- Article
- Airway injury induces alveolar epithelial responses mediated by macrophages.Cell reports · 2026Article
- Immune dysregulation triggered by inflammatory cytokines in patients with severe respiratory infections.Respiratory research · 2026Article
- Stress-induced sympathetic hyperactivation drives hair follicle necrosis to trigger autoimmunity.Cell · 2026Article
- Toll-like receptors in innate immunity and inflammation: from fundamental biology to clinic insights.Immunity & inflammation · 2026Review
- The single-cell immune atlas of bacterial pneumonia: from inflammatory cell infiltration to treatable cell states.Frontiers in cellular and infection microbiology · 2026Review
- Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025Review
Corrections and comments
- Update of
Authors and funding
21 authors.
Funding
Abstract
Tissue repair programs must function alongside antiviral immunity to restore the lung epithelial barrier following infection. We found that macrophage-derived oncostatin M (OSM) counteracted the pathological effects of type I interferon (IFN-I) during infection and damage in mice. At baseline, OSM-deficient mice exhibited altered alveolar type II (ATII) epithelial cell states. In response to influenza or viral mimic challenge, mice lacking OSM exhibited heightened IFN-I responses and increased mortality. OSM delivery to the lung induced ATII proliferation and was sufficient to protect deficient mice against morbidity. Furthermore, OSM promoted organoid formation despite the growth-inhibitory effects of IFN-I. These findings identify OSM as an indispensable macrophage-derived growth factor that maintains the homeostasis of lung epithelial cells and promotes their proliferation to overcome IFN-I-mediated immunopathology.
Indexed as
Identifiers
What OpenQuestion holds
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.