Immune mechanisms of acute and recurrent pericarditis
Pericarditis is increasingly recognized as an inflammatory disease, yet the immune mechanisms that initiate acute pericardial inflammation and drive recurrent disease remain incompletely understood. We investigate the contributions of innate and adaptive immunity to pericarditis using complementary basic and translational approaches. We are developing preclinical models to define the immune pathways that initiate and sustain pericardial inflammation. In parallel, our INFLAME biobank provides longitudinal patient samples from individuals with recurrent pericarditis, enabling us to investigate immune responses across active disease, remission, and treatment. By integrating experimental models with human immunophenotyping, we aim to identify mechanisms that distinguish self-limited inflammation from recurrent disease and uncover new therapeutic targets for patients with pericarditis.
Hypoxia as a driver of cardiovascular disease
Reduced oxygen availability is a central feature of many cardiovascular and cardiopulmonary diseases, yet the mechanisms by which chronic hypoxia drives cardiovascular remodeling remain poorly understood. We investigate how cells and tissues sense and adapt to sustained reductions in oxygen and how these responses become maladaptive in diseases including heart failure with preserved ejection fraction (HFpEF) and pulmonary hypertension. Our work extends beyond canonical oxygen-sensing pathways to identify previously unrecognized molecular and metabolic responses to chronic hypoxia. We seek to determine how these pathways can be manipulated to preserve physiologic adaptation to low oxygen while preventing pathologic cardiac and vascular remodeling.
Inter-organ lipid handling during chronic hypoxia
Our ongoing work has revealed an unexpected interaction between oxygen availability and lipid metabolism. We are investigating how chronic hypoxia alters the storage, utilization, transport, and disposal of lipids across organs, and how dietary lipid composition modifies these responses. By defining these inter-organ pathways, we aim to uncover new mechanisms linking hypoxia and metabolic dysfunction to cardiovascular disease and identify strategies to redirect lipid handling away from vulnerable organs.