Silencing CTGF/CCN2 inactivates the MAPK signaling pathway to alleviate myocardial fibrosis and left ventricular hypertrophy in rats with dilated cardiomyopathy.

Dilated cardiomyopathy (DCM) is characterized by left ventricular dilation associated with systolic dysfunction. The purpose of the current study is to clarify the effect of connective tissue growth factor (CTGF/CCN2) on myocardial fibrosis and left ventricular hypertrophy (LVH) of rats with DCM through the mitogen-activated protein kinase (MAPK) signaling pathway. First, DCM rat models were established and sh-CTGF/CCN2 lentiviral expression vectors were constructed. Then, by observing the pathological changes and myocardial ultrastructure as well as detecting cardiac functions, myocardial fibrosis, and LVH of rats, the effect of CTGF/CCN2 gene silencing on rats with DCM was investigated. To further explore how CTGF/CCN2 gene silencing affects rats with DCM, the expression of CTGF/CCN2 and the related genes of the MAPK signaling pathway was detected. Sh-CTGF/CCN2-2 and sh-CTGF/CCN2-3 with lower CTGF/CCN2 expression were selected for further experimentation. CTGF/CCN2 gene silencing improved cardiac function and alleviated myocardial fibrosis and LVH of rats with DCM. It was also verified that CTGF/CCN2 gene silencing could relieve the pathology of rats with DCM by inactivation of the MAPK signaling pathway. We conclude that CTGF/CCN2 gene silencing inhibits the activation of the MAPK signaling pathway, thus decreases myocardial fibrosis and LVH, and then improves the pathological symptoms of DCM in rats.