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Disruption of Coordinated Angiogenesis and Cardiac Hypertrophy Contributes to the Transition to Heart Failure

机译:协调血管生成和心脏肥大的破坏有助于转变为心力衰竭

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Cardiac hypertrophy is associated with the upregulation of vascular en-dothelial growth factor (VEGF) in the myocardium. We evaluated the effects of a decoy VEGF receptor on heart morphology and function to a murine model of pressure overload hypertrophy. Treatment with adenoviral vector encoding a decoy VEGF receptor (Ad-Flk) led to a net reduction in capillary density in hearts subjected to transverse aortic constriction (TAC). Ad-Flk also led to a reduction in TAC-induced cardiac hypertrophy and promoted left ventricle dilatation and a loss in contractile function. These findings suggest that VEGF is required to maintain myocardial capillary density and that reductions in the vascular bed is associated with the transition from compensatory hypertrophy to failure.
机译:心肌肥厚与心肌中血管脑含量增长因子(VEGF)的上调有关。 我们评估了诱饵VEGF受体对心脏形态学的影响和压力过载肥大鼠模型的作用。 用腺病毒载体治疗编码诱饵VEGF受体(AD-FLK)导致透析横向主动脉收缩(TAC)的心中毛细密度的净降低。 AD-FLK还导致TAC诱导的心脏肥大减少,促进了左心室扩张和收缩功能的损失。 这些发现表明VEGF需要维持心肌毛细血管密度,并且血管床的减少与从补偿肥大失败的过渡相关。

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