Our laboratory is dedicated to advancing the understanding of vascular biology, with a particular emphasis on the mechanisms that drive vascular dysfunction and remodeling in disease. A central focus of our work is hypoxia-induced pulmonary hypertension, a devastating condition characterized by maladaptive changes in the pulmonary vasculature that culminate in elevated pressures and right heart failure. We investigate how low oxygen tension alters cellular signaling and vascular homeostasis, leading to activation, injury, and reprogramming of key vascular cell types, including endothelial cells, smooth muscle cells, pericytes and fibroblasts.

By mapping the molecular interactions and signaling networks that govern these processes, we aim to uncover the drivers of pathological remodeling. In parallel, we are interested in the regenerative capacity of vascular tissues and the potential for cellular reprogramming to restore function. This includes dissecting pathways of vascular regeneration, repair, and plasticity that could be harnessed to reverse damage.

Our integrated approach spans molecular, cellular, and in vivo systems to bridge fundamental biology with translational discovery. Ultimately, the goal of our research is not only to illuminate the underpinnings of vascular pathology, but also to exploit these insights for development of novel therapeutic strategies. By targeting maladaptive signaling and promoting regenerative programs, we strive to pioneer innovative treatments for pulmonary hypertension and other vascular diseases