Abstract 2130 Optimization of fibroblast-selective inhibitors of YAP/TAZ as novel therapeutics for Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and fatal disease in which aberrant fibroblast proliferation, contraction, and extracellular matrix (ECM) deposition causes lung function decline. Studies by our group and others, have identified a pivotal role for Yes-associated protein 1 (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) transcription co-factors in activating fibroblasts to drive fibrosis in the lung. Although these studies highlight the YAP/TAZ transcriptional program as a potential target for drug discovery, the multitude of signaling inputs modulating this pathway, YAP and TAZ ubiquitous expression, and their involvement in a wide array of cell functions, including stem cell maintenance, epithelial and endothelial homeostasis, render them challenging therapeutic targets.