Time-lapse imaging and the modular recreation of host physiology reveal that alveolar epithelial cells, potential permissive infection sites for Mycobacterium tuberculosis, can restrict early bacterial growth via surfactant secretion.

Lung stem cell niche aging is associated with altered bioenergetics, metabolic dysfunction, and senescence of mesenchymal stromal cells that restricts 3D organoid, or alveolosphere formation, potentially accounting for reduced regenerative capacity with aging.

Airway cells are required for the maintenance of the adult mouse lung and for carcinogen-induced lung adenocarcinoma development, and are thus marked therapeutic targets.

Telomere dysfunction in iPSC-derived type II alveolar epithelial cells causes senescence and gene expression changes including Wnt-related changes that GSK3 inhibition can rescue, providing insight into pulmonary fibrosis pathogenesis.

A serum-free organotypic culture model of mouse lung epithelial progenitors was developed and used to screen WNT modulators for regulators of epithelial differentiation.

Regulation of cellular properties such as ligand secretion and migratory ability through changes in the cytoskeleton mediated by a Wnt5a–Ror2–Vangl2 axis is a major determinant of alveolar formation.

Alveolar type 2 stem cells are actively maintained by Hippo signaling and Taz promotes alveolar epithelial regeneration and the resolution of bleomycin induced pulmonary fibrosis upon inactivation of the Hippo pathway in Alveolar type 2 stem cells.

Mitochondrial activity and distribution control alveolar formation by conferring distinct cellular properties.

Publicly available gene expression data and proven methodologies for building model Gene Regulatory Networks are applied to successfully construct the IGF1 signaling GRN behind alveologenesis, serving as a pioneer in transforming how lung development and its associated diseases is approached.

A population of p63⁺ Krt5^- epithelial cells contribute to alveolar regeneration independent of the presence of ectopic tuft cells following viral infection.