关键词: 组蛋白甲基转移酶 Smyd2, 基因敲除, 心肌肥厚, 纤维化, 心脏功能

Abstract: Objective To investigate the effect of SET and MYND domain-containing protein 2 ( Smyd2 ) gene knockout on the development of pathological cardiac hypertrophy induced by pressure overload. Method Ten wildtype mice and 10 Smyd2 knockout mice were randomly divided into pathological cardiac hypertrophic model group. The pathological cardiac hypertrophy was established by transverse aortic constriction ( TAC) surgery in mice. The structure and function of the heart were detected by echocardiography 4 weeks after surgery, and the degree of cardiac hypertrophy and fibrosis was evaluated by histological pathological staining. Result At 4 weeks after aortic arch ligation, the degree of cardiac hypertrophy and fibrosis in Smyd2 knockout mice was significantly higher than that wild-type mice. Ultrasound result showed that Smyd2 knockout increased the impairment of cardiac function caused by stress load. Conclusion Smyd2 deficiency exacerbates pathological myocardial hypertrophy, fibrosis and heart dysfunction induced by stress load.

Key words: Smyd2, gene knockout, cardiac hypertrophy, fibrosis, heart function