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

摘要： 目的 探讨组蛋白甲基转移酶Smyd2基因敲除对压力超负荷诱导的病理性心肌肥厚发生发展的影响。方法 将 10 只野生型小鼠和 10 只Smyd2 基因敲除小鼠采取主动脉弓结扎术建立小鼠病理性心肌肥厚模型,术后4 周超声检测心脏结构和功能,并通过组织学病理染色评价心肌肥厚和纤维化的程度。 结果 主动脉弓结扎术 4周后,与野生型小鼠相比,Smyd2 基因敲除小鼠的心肌肥厚和心脏纤维化程度加重,超声结果显示,Smyd2 敲除加重了压力负荷导致的心脏功能受损。 结论 Smyd2 敲除加重压力负荷导致的病理性心肌肥厚和心肌纤维化,导致心脏功能受损。

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