Single cell transcriptomics reveal a complex orchestration of lung immune cells during the transition from fetal to air-breathing life to fill context-specific functions in tissue remodeling, angiogenesis, and immunity.

The kinin-kallikrein system is a crucial target for the treatment of COVID-19.

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

COVID-19 survivors, who are at risk for vascular complications, would benefit from close monitoring and preventive therapy.

Transcription changes in cells taken from bronchoalveolar fluid of COVID-19 patients indicate severe disruption of coagulation and fibrinolytic pathways in the lung and suggest similar processes in other organs.

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.

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

Single-cell transcriptomic profiling and systematic analysis of pulmonary neuroendocrine cells identifies over 40 hormones and neuropeptides expressed in myriad combinations, and predicts their targets in mouse and human lung, revealing extraordinary sensory and signaling diversity and potential physiological functions.

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.