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Disease Modeling

A critical prerequisite for successful translation to human application is the modeling of cardiovascular disease (CVD) as a complex disease in relevant systems. Within the Munich Heart Alliance network a broad range of established and ongoing in vitro and in vivo models - comprising patient-specific induced pluripotent stem cells as well as small and large animal models - is available.
The focus in this research program will be on vascular inflammation and remodeling as well as on platelet biology.


Vascular inflammation and remodeling

The chronic inflammatory response of the arterial wall hallmarks both early and late stages of CVD. The inhibition of the recruitment of immune cells to the arterial vessel wall could therefore be a promising strategy to treat and prevent CVD. One goal of the Munich Heart Alliance is to identify and target processes that are specifically related to vascular inflammation in CVD and develop drug candidates without adverse immunological effects.
We characterize inflammatory responses on a cellular level by novel imaging approaches and dissect mechanisms underlying remodeling and microcirculatory disturbances. Advanced intravital microscopy is employed to address the question to what extent impairment of microcirculatory blood flows affects development or progression of macrovascular disease.


Platelet biology and thrombosis

Dysregulation of thrombosis and haemostasis are considered key events both in the manifestation of advanced CVD and also in the initiation of the atherosclerotic process itself. While efficient anti-thrombotic strategies have been integrated into daily clinical management of CVD patients, these approaches are non-specific since they also target normal haemostasis and hence are associated with considerable bleeding complications. To develop novel strategies that prevent atherothrombosis at minimized effects on normal haemostasis, one of the major challenges of MHA research network is to gain a better understanding of the molecular and cellular mechanisms underlying thrombotic complications of CVD.