ArticleBMC pulmonary medicine2026
Type II alveolar epithelial cell-specific CAP1 loss is associated with spontaneous pulmonary fibrosis and altered complement 5 signaling.
Article in BMC pulmonary medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Abstract
backgroundCyclase-associated protein 1 (CAP1) is widely expressed in mammalian tissues; however, its physiological role in the lung remains largely unclear. This study aimed to explore the function of CAP1 in alveolar type 2 (AT2) cells and its potential association with pulmonary fibrosis. METHODS AND
resultsAn inducible AT2 cell-specific CAP1 conditional knockout mouse model (CAP1
conclusionsThese findings indicate that CAP1 deficiency in AT2 cells is associated with spontaneous fibrotic remodeling and altered complement signaling in the lung. The data support a model in which CAP1 loss may perturb AT2 cell homeostasis and local C5 expression, potentially contributing to fibrotic progression. Further studies are required to clarify the causal relationships and underlying mechanisms.
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