Our lab investigates the genetic, cellular, and molecular mechanisms underlying the development of pulmonary arterial hypertension (PAH)- a progressive and life-threatening disease. We aim to understand how pulmonary arteries respond to injury and to identify novel genetic modifiers whose dysfunction may lead to small vessel loss and vascular remodeling in PAH patients.

Using cutting-edge multiomics approaches to explore how various genes and proteins regulate the behavior of pulmonary microvascular endothelial cells (PMVECs) and pulmonary pericytes following vascular injury. Our research also examines changes in cardiac endothelial cells and cardiac pericytes during right ventricular adaptation and damage in PAH.

To better understand disease mechanisms, we utilize transgenic animal models to study disease-associated mutations and how they affect key signaling pathways linked to PAH development.

A central theme of our research is understanding interaction between endothelial cells and pericytes, which is critical for maintaining blood vessel stability. We have also expanded our research to explore how vascular cells communicate through secreted factors, especially extracellular vesicles and exosomes. Our ultimate goal is to discover biomarkers and therapeutic targets that can support the development of innovative diagnostics and treatments for patients living with this devastating condition.