WAGNER

The primary interest of our research is to understand how vessels grow and re-model. As besides endothelial cells, different cell types, e.g. hematopoietic progenitor and myeloid derived cells, pericytes, and smooth muscle cells are involved in vessel formation and maturation, we are interested in the contribution of these different cell types for vessel formation under physiological and pathological conditions. Furthermore, we want to identify signals from surrounding tissues, e.g. myocardium, tumour stroma and immune cells, which modify vessel growth. Finally, the aim of our projects is to translate our findings into potential novel therapeutic approaches and to identify new  pharmacological candidates to modify vascular growth.

The cardiovascular system is the first functional organ system required for embryonic survival. Many major diseases and pathophysiological processes are associated with vessel formation, e.g. coronary artery disease, peripheral arterial diseases, liver fibrosis, wound healing, graft rejection, or cancer. Chronic ischemic heart disease, myocardial infarction, and cancer are the most common causes for morbidity and mortality. In ischemic heart disease, angiogenesis is required for collateral vessel formation and therefore a “friend”, in cancer it becomes a “foe” by inducing the transition of a tumour from a small cluster of malignant cells to a macroscopic tumour capable of spreading to other organs via the vasculature.

We use mainly analyses in mice in vivo (reporter and lineage tracing strains, inducible knockout / overexpression / knockin mice).

The in vivo data are supported by cell culture systems and molecular approaches. We use CRISPR/Cas9 technology to generate reporter cell lines, which serve to test small molecule libraries for their potential to inhibit / activate genes of interest.