Jason X.-J. Yuan, MD, PhD
Photo: Jason X.-J. Yuan
Elected 2007

Dr. Jason Yuan is Professor and Director of the Section of Physiology at the Division of Pulmonary, Critical Care and Sleep Medicine in the University of California, San Diego. The overall research interest of Dr. Yuan’s laboratory is pulmonary vascular pathobiology and genetic, cellular and molecular mechanisms of pulmonary vascular disease, with particular emphasis on the pathogenic role of ion channels and membrane receptors in the development and progression of idiopathic pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension. Dr. Yuan’s research is best demonstrated through his studies on the role of voltage-gated potassium channels and transient receptor potential channels in the development of sustained vasoconstriction and excessive pulmonary vascular remodeling in patients with pulmonary arterial hypertension. Using the combined techniques of patch clamp, digital imaging fluorescence microscopy and molecular biology, his laboratory has defined a critical role of potassium channels in hypoxic pulmonary vasoconstriction, an important physiological mechanism that maximizes oxygenation of venous blood. His work has been integral in demonstrating a pathogenic role for potassium channel dysfunction and downregulation in sustained pulmonary vasoconstriction and excessive pulmonary vascular medial hypertrophy. Furthermore, his laboratory was the first to demonstrate that the upregulation of certain transient receptor potential channels (e.g., TRPC6) and G protein-coupled receptors (e.g., CaSR) is involved in the development of pulmonary vascular remodeling in patients with idiopathic pulmonary arterial hypertension. Dr. Yuan’s work has evaluated both normal and diseased tissues and cells isolated from normal subjects and patients with pulmonary hypertension, allowing for a better understanding of the factors that are directly relevant to the clinical condition. More recently, Dr. Yuan’s research has been focused on elucidating the pathogenic and genetic mechanisms involved in chronic thromboembolic pulmonary hypertension and right heart dysfunction associated with severe pulmonary hypertension.