University of Illinois at Chicago (UIC)
Dr. Youyang Zhao is a Professor of Pharmacology at the University of Illinois at Chicago (UIC). He has completed his B.S. from Fudan University and Ph.D. from Shanghai Institute of Biochemistry, the Chinese Academy of Sciences, and received his postdoc training in cardiovascular biology at Harvard University and UCSD. Prior to his tenure at UIC, Dr. Zhao was a Senior Research Scientist in cardiovascular drug discovery in Pharmacia/Pfizer Inc. Dr. Zhao's research is focused on lung and vascular biology to delineate the molecular mechanisms of endothelial regeneration and resolution of inflammatory injury, as well as pulmonary vascular remodeling in the pathogenesis of pulmonary arterial hypertension (PAH), and thereby to provide novel druggable targets and therapeutic strategies for treatment of acute respiratory distress syndrome and PAH. Dr. Zhao has published many papers in top-tier journals such as Nat Med, PNAS, J Clin Invest, J Exp Med and Circulation. His lab is well-funded with multiple R01 grants and PPG grant from NIH. Dr. Zhao has served as a reviewer for NIH, DOD, and AHA grant applications and many journals.
Recovery of endothelial barrier integrity after vascular injury is vital for endothelial homeostasis and resolution of inflammation. Endothelial dysfunction plays a critical role in the initiation and progression of vascular diseases such as acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and atherosclerosis. A part of the research in the lab, employing genetically modified mouse models of human diseases, endothelial progentior cells/stem cells, and translational research approach as well as nanomedicine, is to elucidate the molecular mechanisms of endothelial regeneration and resolution of inflammatory injury and determine how aging and epigenetics regulate these processes (J Clin Invest 2006, 116:2333; J Exp Med 2010, 207:1675; Circulation 2016, 133:2447). We are also studying the role of endothelial cells in regulating macrophage functional polarization and resolving inflammatory lung injury. These studies will identify druggable targets leading to novel therapeutic strategies to activate the intrinsic endothelial regeneration program to restore endothelial barrier integrity and reverse edema formation for the prevention and treatment of ARDs in patients. Pulmonary hypertension is a progressive disease with poor prognosis and high mortality. We are currently investigating the molecular basis underlying the pathogenesis. We have recently identified the first mouse model of PAH with obliterative vascular remodeling including vascular occlusion and formation of plexiform-like lesions resembling the pathology of clinical PAH (Circulation 2016, 133:2447). Our previous studies also show the critical role of oxidative/nitrative stress in the pathogenesis of PAH as seen in patients (PNAS 2002, 99:11375; J Clin Invest 2009, 119:2009), With these unique models and lung tissue and cells from IPAH patients, we will define the molecular and cellular mechanisms underlying severe vascular remodeling and provide novel therapeutic approaches for this devastating disease.