The focus of Dr. Kass' lab is Idiopathic Pulmonary Fibrosis (IPF). It is a progressive, scarring of the alveolar parenchyma that ultimately leads to respiratory failure and death. Pathologically, this disease is characterized by the unremitting accumulation of fibroblasts. These are the cells responsible for the deposition of extracellular matrix in pulmonary fibrosis.
To gain insight into the pathogenesis of IPF, Dr. Kass' colleagues performed gene expression profiling of IPF lungs compared to normal controls. Dr. Kass has focused on the genes that exhibited increased expression in IPF under the rationale that genes that are highly expressed in IPF likely contribute to the development of pulmonary fibrosis. Specifically, the lab has focused on MetAP2 and Twist1.
Dr. Kass made the novel insight that the MetAP2 expression is necessary for fibroblast proliferation in vitro and that inhibition of MetAP2 with the drug fumagillin suppresses bleomycin-induced pulmonary fibrosis in mice by selectively decreasing the proliferation of fibroblasts in the lung. Upcoming works include testing fumagillin in animal models of pulmonary hypertension.
