Idiopathic pulmonary fibrosis (IPF), a deadly lung disease of unclear etiology, lacks sufficient therapeutic options. We extensively mapped the spatial transcriptomes of patient lungs and made translational comparisons with a mouse model of lung fibrosis, providing insights into disease mechanisms and the utility of the animal model for drug discovery.
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References
Richeldi, L., Collard, H. R. & Jones, M. G. Idiopathic pulmonary fibrosis. Lancet 389, 1941–1952 (2017). A review article that describes IPF pathophysiology, diagnosis, and therapies.
Jenkins, R. G. et al. An official American Thoracic Society workshop report: use of animal models for the preclinical assessment of potential therapies for pulmonary fibrosis. Am. J. Respir. Cell Mol Biol. 56, 667–679 (2017). A report from the American Thoracic Society on available preclinical models for pulmonary fibrosis, affirming the bleomycin mouse model as the best-characterized model.
Habermann, A. C. et al. Single-cell RNA sequencing reveals profibrotic roles of distinct epithelial and mesenchymal lineages in pulmonary fibrosis. Sci. Adv. 6, eaba1972 (2020). This paper reports single-cell RNA-seq data on human IPF lungs, in which they identified the KRT17+KRT5− cell type.
Adams, T. S. et al. Single-cell RNA-seq reveals ectopic and aberrant lung-resident cell populations in idiopathic pulmonary fibrosis. Sci. Adv. 6, eaba1983 (2020). This paper reports single-cell RNA-seq data on human IPF lungs, in which they identified the AbBa cell type.
Strunz, M. et al. Alveolar regeneration through a Krt8+ transitional stem cell state that persists in human lung fibrosis. Nat. Commun. 11, 3559 (2020). This paper reports time-resolved single-cell RNA-seq data from the bleomycin mouse model, resulting in identification of the Krt8+ ADI cell type.
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This is a summary of: Franzén, L. et al. Mapping spatially resolved transcriptomes in human and mouse pulmonary fibrosis. Nat. Genet. https://doi.org/10.1038/s41588-024-01819-2 (2024).
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Mapping the lung fibrosis transcriptome of mice and men. Nat Genet (2024). https://doi.org/10.1038/s41588-024-01833-4
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DOI: https://doi.org/10.1038/s41588-024-01833-4
