Zea Borok

The paper identifies mesothelial cell plasticity as a key determinant of regenerative versus degenerative lung repair by comparing pneumonectomy and chronic lung allograft dysfunction models.

This study identifies age-related epigenetic changes in AT2 cells that promote basal cell metaplasia, contributing to idiopathic pulmonary fibrosis.

The paper identifies regeneration-associated transitional progenitors (RATPs) in Cldn18 knockout mice, showing they are less fibrogenic and contribute to lung repair rather than fibrosis.

The paper creates a high-resolution multimodal lung atlas using single-nucleus RNA and chromatin data from 11 healthy adults, identifying 70 cell populations and 332,846 chromatin regions.

This study shows that the cell of origin in lung adenocarcinoma affects the immunosuppressive state of the tumor microenvironment, with AT1-derived tumors showing an anti-tumor immune profile and AT2-derived tumors showing immunosuppressive features.

The paper identifies TRIP13 as a mediator of AT2 cell dysfunction in IPF through integrated transcriptomic and epigenomic analysis and shows TRIP13 inhibition prevents mesenchymal gene signature acquisition.

The paper identifies GRAMD2+ alveolar type I cells as plastic and capable of transitioning through multiple lung epithelial cell states in organoid culture.

The paper constructs a gene regulatory network (GRN) for alveologenesis in a mouse model of BPD, revealing how IGF1 signaling regulates lung development and identifies potential therapeutic targets.

This study identifies key epigenetic states and transcription factor networks in human alveolar epithelial differentiation, revealing dynamic enhancer changes and regulatory interactions critical for distal lung identity.

The paper shows that Vegfa from alveolar type 1 cells specifies a distinct endothelial population in the mouse lung, marked by Car4 and involved in alveologenesis.