The ablation of VEGFR-1 signaling promotes pressure overload–induced cardiac dysfunction and sudden death. The ablation of VEGFR-1 signaling promotes pressure overload–induced cardiac dysfunction and sudden death

Deletion of VEGFR-1 signaling appears not to have an effect on normal cardiac function but it inhibits the development of early compensatory LVH, which in turn leads to diastolic dysfunction associated with atrial dilatation and increased risk of sudden cardiac death Overall design: Cardiac mRNA profiles after AngII induced left ventricular hypertrophy in VEGFR-1 tyrosine kinase knockout and littermate control mice