Research Project: Catecholamine Signaling Regulates Pulmonary Fibrosis
Idiopathic pulmonary fibrosis (IPF) is an aggressive and fatal disease that causes scarring (fibrosis) of the lungs. Scarring causes stiffness in the lungs and makes it difficult to breathe. Lung damage from IPF is irreversible and progressive, meaning it gets worse over time. The processes that promote the chronic nature and prevent resolution of pulmonary fibrosis are not understood. We will investigate the role hormones called catecholamines (dopamine, norepinephrine and epinephrine) play in regulating pulmonary fibrosis. We will study how catecholamine cell signaling regulates the disease and test clinically approved drugs which regulate catecholamines in models of pulmonary fibrosis. The results could lead to a potential treatment that not only halts the progression of fibrosis but promotes its reversal and improves lung function.
Over the past year we have continued investigating catecholamine signaling as a means to promote lung fibrosis resolution. We have discovered that all three catecholamines: dopamine, norepinephrine, and epinephrine lead to inhibition of cell-signaling pathways that are known to play a major role in activating lung fibroblasts, which leads to fibrosis. Based on these findings we are now testing which clinically approved inhibitors of catecholamine metabolism could serve as an effective therapy for IPF.