ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
A Human Immuno-Lung Organoid Model to Study Macrophage-Mediated Lung Cell Senescence Upon SARS-CoV-2 Infection.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
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
4 citing papers in PubMed.
- Dissecting human organ development using spatial technologies.Developmental cell · 2026Review
- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
- Organoids for disease modeling and treatment: state-of-the-art.Experimental hematology & oncology · 2026Review
- A Human Immuno-Lung Organoid Model to Study Macrophage-Mediated Lung Cell Senescence Upon SARS-CoV-2 Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
25 authors.
Funding
Abstract
While COVID-19 affects multiple organ systems, the human respiratory system is the primary viral target and main site for disease progression. In this study, spatial transcriptional assays (NanoString CosMx) are utilized to analyze both explant and autopsy samples from non-COVID and COVID-19 lungs, identifying the activation of proinflammatory macrophages in COVID-19 explants. It is further developed immuno-lung organoids comprising hPSC-derived alveolar and airway organoids co-cultured with macrophages to investigate the impact and underlying mechanisms of macrophage-mediated lung damage following SARS-CoV-2 infection. The findings demonstrate that proinflammatory macrophages induce lung cell senescence through the THBS1-(ITGA3+ITGB1) signaling axis, a mechanism further validated using spatial transcriptomics. This study not only establishes physiologically relevant immuno-lung organoid models for modeling macrophage-mediated tissue damage, but also identifies a previous unrecognized role of the THBS1-(ITGA3+ITGB1) pathway in driving lung cell senescence during infectious disease.
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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 Socratic graph.