Autoimmunity at the crossroad of coagulation and inflammation in Atrial Fibrillation

Saskia C.A. de Jager & Suzanne J.A. Korporaal

There is mounting evidence that, in addition to hypercoagulability, inflammation is an important contributor to atrial remodeling and AF development. Apart from that AF includes endothelial damage, which is reflected by the presence of autoantibodies directed against endothelial cells. Anti-endothelial cell autoantibodies can form immune-complexes, bind to damaged endothelium and induce platelet aggregation and subsequent thrombus formation.

Beyond their prominent role in hemostasis and thrombosis, platelets are increasingly recognized as being key players in several other biological disease processes, like fibrosis and immune regulation. Platelets interplay with damaged endothelium, interact with immune cells, provide the surface for activation of the coagulation system, and are the storage site of bioactive molecules involved in tissue injury and remodeling. Thus, plateletsmay be the key connecting inflammation with the progression of AF.

We hypothesize that the presence of chronic inflammation triggers auto-immune responses targeting the dysfunctional endothelium, thereby providing a substrate for platelet activation, culminating in an active contribution to the onset and progression of AF.

With this research grant, we will be able to create the fundament of our collaborative research line on the crossroad of autoimmunity and platelet-dependent responses in cardiovascular disease, which hopefully will create opportunities to generate additional funding.  

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