ArticleThe Journal of clinical investigation2025
Stress, plasticity, and fibrosis: unfolding the role of the IRE1α/RIDD/Fgfr2 axis.
Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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1 citing paper in PubMed.
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1 author.
Funding
Abstract
Recent advances in sequencing technologies have enabled the identification of intermediate cell states during alveolar epithelial differentiation, which expand during repair following injury and in fibrotic lungs. Although ER stress has been implicated in pulmonary fibrosis, the underlying mechanisms remain elusive. The featured study by Auyeung and colleagues looked for links between the unfolded protein response sensor inositol-requiring enzyme 1α (IRE1α), intermediate epithelial cell states, and fibrotic remodeling in the lung. They identified Regulated IRE1-Dependent Decay (RIDD) as a key effector of IRE1α signaling that drives differentiation of alveolar epithelial type 2 cells to damage-associated intermediate cells and contributes to pulmonary fibrosis, likely by degrading Fgfr2 mRNA. These findings unveil therapeutic targets and open new avenues for investigating the interplay between cellular stress responses, epithelial differentiation, and fibrotic disease.
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