B06-Modification of PI 3-kinase signalling as a therapeutic strategy against aortic aneurysm formation

During abdominal aortic aneurysm (AAA) development and disease progression, proliferative smooth muscle cells (SMCs) undergo complex structural and functional changes, which are controlled by receptor tyrosine kinases (RTKs). The PI 3-kinase (PI3K) isoform p110α converges the signals downstream of multiple RTKs. We demonstrated that a lack of p110α in SMCs promotes AAA disease in mice. Therefore, we hypothesise that stimulation of the p110α signalling pathway or modulation of relevant downstream signalling components exert beneficial effects on AAA disease. We will analyse the impact of PTEN as well as FOXO1 inactivation on AAA disease in mice to enable the development of new treatment options.