A07
iNOS- and NoxO1-based redox signaling in COPD-associated PH – pathomechanisms and therapeutic exploitation
Lung vascular alterations and pulmonary hypertension (PH) have been implicated in the development of emphysema and COPD, and PH correlates with patient survival. Our current work provided evidence that iNOS in macrophages drives cigarette smoke-induced PH and that this process critically depends on NoxO1-mediated formation of superoxide. We now aim to 1) delineate the pathogenic phenotype of macrophages involved in development of pulmonary vascular alterations 2) understand the role of iNOS- and NoxO1-based redox signaling in the communication between lung cell types and recruited (pathogenic) macrophages 3) evaluate pharmacological options targeting the iNOS/NoxO1 signaling as the potential treatment strategy for COPD-PH.
