细胞凋亡
缺氧(环境)
细胞生物学
半胱氨酸蛋白酶3
半胱氨酸蛋白酶
锡尔图因
细胞
程序性细胞死亡
半胱氨酸蛋白酶2
生物
化学
生物化学
乙酰化
基因
有机化学
氧气
作者
Ban Liu,Wenliang Che,Jinsong Xue,Changzhu Zheng,Kai Tang,Jingying Zhang,Jing Wen,Yawei Xu
摘要
Aims: Apoptosis plays a critical role in cardiomyocyte loss during ischaemic heart injury. A detailed understanding of the mechanism involved has a substantial impact on the optimization and development of treatment strategies. Here, we report that the expression of SIRT4, a mitochondrial sirtuin, is markedly down-regulated in hypoxia-induced apoptosis of H9c2 cardiomyoblast cells. Methods and Results: SIRT4 interference significantly alters H9c2 cell viability, apoptotic cell number and caspase-3/7 activity. Furthermore, SIRT4 expression can affect the ratio of pro-caspase 9/caspase 9 or pro-caspase 3/caspase 3, an affect Bax translocation, which in turn alters the development of H9c2 cell apoptosis. Conclusion: These results suggest that SIRT4 is a key player in hypoxia-induced cardiomyocyte apoptosis, and that strategies based on its enhancement might be of benefit in the treatment of ischaemic heart disease.
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