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

血管内皮生长因子受体1 (VEGFR-1) 信号通路的缺失对正常心脏功能似乎无影响，但可抑制早期代偿性左心室肥厚 (Left Ventricular Hypertrophy, LVH) 的发生发展，进而引发与心房扩张相关的舒张功能障碍，并增加心源性猝死风险。
整体实验设计：在血管紧张素II (Angiotensin II, AngII) 诱导左心室肥厚的小鼠模型中，对VEGFR-1酪氨酸激酶敲除小鼠及其同窝对照小鼠的心脏mRNA表达谱进行检测。