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Restores Epithelial Identity and Mitigates Lung Fibrosis

ABSTRACT: In this study, we investigated how S100A2 overexpression, hypoxic stress, and 2D monolayer culture conditions disrupt the epithelial identity of human iPSC-derived alveolar type 2 cells (iAT2s), a key pathological feature of lung fibrosis. Using defined perturbations, we examined how each factor contributes to cellular reprogramming, loss of AT2 fate, and induction of stress-responsive or basal-like transcriptional states. Together, these analyses provide mechanistic insight into how microenvironmental and molecular cues drive AT2 cell dysfunction during fibrotic remodeling.

ORGANISM(S): Homo sapiens

PROVIDER: GSE311800 | GEO | 2025/12/08

REPOSITORIES: GEO

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