Authors
Nicole Foxworth, Julie Wells, Sara Ocana-Lopez, S Muller, Pooja Bhayani, James Denegre, Kristina Palmer, Wendy Memishian, Teresa McGee, Stephen A Murray, Patricia K Donahoe, Carol J Bult, Maria Loscertales
Published in
eLife. Volume 13. Oct 12, 2026. Epub Oct 12, 2026.
Abstract
Disruptions in airway branching or alveolar differentiation during lung development can lead to severe respiratory deficiencies and neonatal death. The molecular mechanisms governing branching patterning and early alveolar formation remain elusive. Loss of Svep1 function in mice results in various developmental defects, including lung hypoplasia and perinatal lethality. Our examination of the lungs of Svep1 knockout (Svep1-/-) mouse embryos, both in vivo and in vitro, revealed that Svep1 mutants exhibit an increase in the number of disorganized distal airway tips, progressively greater disruption of lung lobe morphology over time, and disrupted saccular development. Svep1 interacts with FGF signaling to regulate smooth muscle differentiation and, together with Fgf9, guides airway branching patterning. Transcriptomic data from the lungs of Svep1-/- embryos revealed dysregulated gene expression affecting saccular maturation. Our findings demonstrate that Svep1 is a key extracellular matrix player shaping airway morphology and influencing alveolar fate. These insights offer potential avenues for therapeutic interventions in congenital lung disorders.
PMID:
42862199
Bibliographic data and abstract were imported from PubMed on 12 Oct 2026.
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