Johannes HOLFELD
Universitätsklinik für Herzchirurgie
Medizinische Universität Innsbruck
Website

Program

"Targeting the innate immunity in cardiovascular disease"

Innate immune receptor Toll-like receptor 3 (TLR3) has been described to increase epigenetic plasticity thereby enabling transdifferentiation of interstitial cells to mesenchymal cells.
This mechanism occurs to be a relevant pathomechanism as well as a therapeutic avenue. The cardiosurgical research lab at Medical University of Innsbruck has discovered the XYLT1-BGN-TLR3 axis to be responsible for development of aortic valve calcification. This finding enables for a potential pharmacological intervention, which is currently under investigation. In parallel, a single and short stimulation of TLR3 in the myocardium induces trensdifferentiation of cardiac fibroblasts to vessel forming endothelial cells. This new approach has alread led to a clinical trial in patients suffering from ischemic cardiomyopathy. It has shown convincing results regarding improvement of left ventricular ejection fraction (LVEF) and is close to entering clinical routine.

Host: Johannes SCHMID

Contact for questions: Helmut KUBISTA