My research line focuses on microvascular dysfunction in cardiometabolic diseases, ultimately resulting in vital organ failure. Specifically, I aim to elucidate the role of fat tissue around arteries, or perivascular adipose tissue (PVAT), in metabolic and contractile muscle function. This research started with a hypothesis paper published in The Lancet and has resulted in evidence that PVAT controls muscle blood flow through a balance of vasodilator and vasoconstrictor products, i.e. adipokines. While the balance between these two is tilted towards vasodilator adipokines in normal physiology, it shifts towards vasoconstrictor adipokines in human and experimental obesity, preceding symptoms of diseases such as type 2 diabetes.  My group has also shown that kidney failure, a complication of obesity and diabetes, has a separate and aggravating effect on organ blood flow through reduction of the synthesis of nitric oxide.

                After starting my research on microvascular dysfunction in muscle, I have translated this mechanistic knowledge to cardiac diseases associated with type 2 diabetes and impaired microvascular function, i.e. ischemia with no obstructed coronary arteries (INOCA) and HFpEF. In these studies I study mechanisms that reduce tissue blood flow in non-obstructive coronary artery disease and heart failure with preserved ejection fraction. In this research I collaborate with cardiologists and endocrinologists.

                In a recently awarded consortium grant from the Netherlands Organisation for Scientific Research (3-2-Tango), a team of 9 scientists in Amsterdam and Maastricht that I lead investigates the role of perivascular adipose tissue in regulation of microvascular function and insulin sensitivity. This research features imaging of human muscle research in vivo, co-culture modeling of skeletal muscle as described in WP1.1 and nanomedicine treatment of PVAT inflammation.

Microcirculation

Type 2 diabetes

Obesity

Muscle 

Myocardial ischemia