My research investigates the role of the endothelium (the lining of the blood vessels) in systemic sclerosis-associated interstitial lung disease (SSc-ILD), a fibrotic lung complication of systemic sclerosis and the leading cause of death in this autoimmune disease. Because vascular injury is among the earliest events in systemic sclerosis, often appearing well before the lung is visibly scarred, my work focuses on how endothelial dysfunction drives the development of fibrosis. A central interest is endothelial RIPK3, a kinase best known as a driver of necroptosis, a form of regulated, inflammatory cell death.

Using the bleomycin-induced mouse model of pulmonary fibrosis, endothelial-specific knockout mice, cell culture systems, and proteomic and transcriptomic approaches, my studies examine how RIPK3 activity within endothelial cells contributes to the loss of normal vascular function and to the progression of lung fibrosis. My long-term goal is to identify vascular mechanisms that could be targeted therapeutically before irreversible scarring occurs, with implications that may extend to other inflammatory and fibrotic diseases in which endothelial dysfunction plays a role.