Cardiovascular disease such as heart attack, stroke, and peripheral vascular disease, is the number-one health problem in the world. Despite remarkable progress in diagnosis and prevention, cardiovascular diseases cause disability and death at an astounding rate. The best opportunities to develop and implement new strategies for preventing and treating cardiovascular disease lies in the understanding of its underlying mechanisms. Our research aims to isolate novel therapeutic targets that effectively prevent and most importantly, also reverse complications mediated by cardiovascular risk factors such as hypertension.

Specifically, we are interested in sphingosine-1-phosphate (S1P) signaling and its role in the regulation of the vascular and the immune system. Our earlier work provides ample evidence that the S1P signaling axis plays a key role in immune cell recruitment, cytokine production and vascular tone regulation in experimental hypertension, heart failure and stroke. We for instance, showed an essential contribution of the S1P signaling axis to hypertension by identifying hematopoietic SphK2 as key enzyme responsible for disease-associated S1P plasma elevation that governs T-cell egress from secondary lymphoid tissue and thus, controls BP. On the other hand, S1P signaling involves in heart-failure and stroke associated cerebrovascular alterations that link to cerebral blood flow deficits and neurodegeneration, including memory deficits. Interestingly, targeting S1P signaling pathways specific to the different diseases improve disease outcome.