Telomerase gene therapy represents a novel effective treatment for pulmonary fibrosis associated with short telomeres by improving pulmonary function, decreasing inflammation and accelerating fiber disappearance in fibrotic lungs.

Single-cell RNA sequencing reveals extensive endothelial cell (EC) heterogeneity throughout the lung vasculature and identifies two distinct populations, Car4-high ECs and proliferative ECs, that preferentially respond to lung injury.

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.

RNA profiles from lungs of mice exposed to intermittent hypoxia shared similarity with gene expression changes in human lung from patients with pulmonary diseases, including pulmonary hypertension, COPD, and asthma.

Influenza-induced pulmonary tuft cells are a heterogenous population and emerge independently of Type 2 and interferon signaling, and do not impact dysplastic epithelial regeneration.

Hyperglycaemia increases influenza severity by damaging the pulmonary epithelial-endothelial barrier and increasing pulmonary oedema during Influenza A virus infection.

After acute lung injury, the transcription factor Atf3 is essential for regeneration of the capillary endothelium, which is critical for restoring the structure of the lung alveolus.

Endothelial pannexin 1-P2Y2 purinergic receptor-TRPV4 channel signaling, facilitated by caveolin-1, is a novel pathway for lowering pulmonary arterial pressure.

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

An induced pluripotent stem-cell-based, human heart and lung co-differentiation model reveals their shared signaling requirement and enables investigation of their developmental mutual interaction and tissue boundary formation.