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.

Disrupted mesenchymal Bmpr1a-mediated signaling in fetal mouse lung leads to abnormal airway development and congenital pulmonary cyst formation.

Lineage tracing using a knockin Pdgfra-rtTA tool indicates distinct contributions of this cell lineage to myofibroblasts in normal development, fibrosis and bronchopulmonary dysplasia models.

Directed differentiation of stem cells can generate ventral-anterior foregut spheroids that can expand into three-dimensional lung organoids with striking structural, cellular and molecular similarities to the human fetal lung.

Oxygen-independent (pseudohypoxic) HIF pathway activation is a core determinant of dysregulated collagen-structure function in human fibrosis.

Inhibition of a single fibroblast-associated transcription factor, namely Paired-related Homeobox Protein 1 (PRRX1), is sufficient to dampen lung fibrogenesis.

The Foxa2 lineage-based organ generative strategy allows us to establish a unique paradigm for the simultaneous generation of functional whole lungs and thymus, which can be applied to future transplantation therapy.

Tsc2 inactivation in mouse mesenchymal progenitors produced tumors with vascular anomalies reminiscent of human angiomyolipomas, and a gene expression signature in Tsc2-deficient tissues which included Lgals3, as a novel potential biomarker for TSC1/2 loss.

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

Erlotinib-resistant AXL overexpressing cells are present in therapy-naive tumors, and expression of AXL in these cells is regulated through a stochastic mechanism centered on the epigenetic regulation of miR-335.