心肌肥大/凋亡是肺动脉高压综合征（PHS）肉鸡的主要病理学特征，也是肉鸡PHS形成的关键环节。初步研究发现PHS肉鸡心肌细胞肥大/凋亡过程中ARC蛋白表达水平明显下降，提示ARC蛋白的不足或耗竭可能是心肌细胞肥大/凋亡形成的主要机制。有研究表明ARC抗心肌肥大/凋亡是通过Caspases通路实现的，而ARC蛋白在肉鸡PHS形成的过程中是如何作用的及其作用机制未见报道。本研究拟运用肉鸡心肌细胞肥大/凋亡模型，通过导入ARC过表达载体及siRNA实现对ARC蛋白的过表达或抑制，并结合外源性ARC在体实验，运用荧光定量PCR，western-blot、免疫荧光、免疫沉淀等方法探索ARC蛋白经Caspases通路调控PHS肉鸡心肌细胞肥大/凋亡的分子机制，为深入研究肉鸡PHS的病理发生和防治提供新的实验依据。

Myocardial hypertrophy / apoptosis is the main pathological feature of PHS and the key link of PHS formation. This laboratory's previous study found that the expression level of ARC protein decreased significantly during the mast / apoptosis of cardiac myocytes in PHS broilers. The results suggested that the deficiency or depletion of ARC protein may be the main mechanism for the formation of hypertrophy / apoptosis in cardiomyocytes. Studies have shown that ARC's anti-myocardial hypertrophy / apoptosis is achieved through the Caspaise pathway, and how the ARC protein functions in this process and its mechanism have not been reported. In this study, insulin/hypoxic induction was used to establish a model of hypertrophy and apoptosis in broiler cardiomyocytes. The expression or inhibition of ARC protein was achieved by introducing ARC hyperexpression vector and siRNA, and combined with the addition of exogenous ARC and PHS broiler. In vivo experiments, Using fluorescence quantitative PCR, western-blot, immunofluorescence and other methods to explore the molecular mechanism of the regulation of hypertrophy / apoptosis of cardiac myocytes in PHS broilers via Caspades pathway of ARC protein.To provide a new experimental basis for further study on the pathogenesis and prevention of PHS in broilers.