About Dr. Zea Borok

Since alveolar epithelial type II (AT2) cells serve as stem/progenitor cells for adult alveolar epithelium, understanding the mechanisms that regulate their self-renewal and transdifferentiation to a type I (AT1) cell phenotype are key to understanding mechanisms of repair following injury, as well as aberrant AEC differentiation and failure of re-epithelialization which appears central to disease pathogenesis (e.g., in IPF).

For our studies, we utilize complementary in vitro and in vivo models including rat, mouse and human AEC in primary culture, lung injury models (e.g., bleomycin, hyperoxia and lipopolysaccharide) and genetically modified rats and mice (including novel cell-specific Cre lines) as well as genome-wide genomic and epigenomic technologies.