ArticleInflammation and regeneration2025
Ex vivo lung-organoid model for aberrant basaloid cell induction and activation.
Article in Inflammation and regeneration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Aberrant and ectopic cell populations in restrictive allograft syndrome after lung transplantation.The European respiratory journal · 2026Article
- A multifunctional ICAM1-directed MnO₂@ZIF8 nanoplatform with Tanshinone IIA synergistically reverses senescence and restores alveolar regeneration in septic lung injury.Journal of nanobiotechnology · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundPulmonary fibrosis (PF) is a severe lung disease characterized by the destruction of lung architecture resulting from chronic epithelial injury. The PF microenvironment induces PF-specific epithelial cells, such as aberrant basaloid cells (ABCs). However, limited experimental models capable of inducing and activating PF-specific epithelial cells hinder the understanding of their roles.
methodsTo address the lack of experimental models, in this study, we developed an ex vivo murine lung-organoid model designed to induce and activate ABCs. The organoids were subjected to bleomycin (BLM) stimulation. Dose-dependent reductions in number and size, structural disorganization, and transcriptomic changes were assessed following stimulation. Single-cell RNA-sequencing (scRNA-seq) analysis was performed to identify ABC subsets. Cell-cell interaction analysis was also conducted.
resultsFollowing BLM stimulation, the organoids displayed dose-dependent reductions in number and size, along with structural disorganization and transcriptomic changes that were similar to those observed in the in vivo murine fibrosis model. scRNA-seq analysis identified two ABC subsets: Krt5
conclusionsThe developed organoid model serves as a novel platform for studying the roles and responses of PF-specific ABCs. This model may contribute to advancing the understanding of PF pathogenesis and facilitate the development of ABC-targeted therapies.
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