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Title:: Progress on protective mechanism of AMPK against myocardial ischemia

作者:: 钱晨曦; 徐洁晨; 张琳综述; 余志斌审校; （第四军医大学航空航天生理学教研室，陕西西安 710032）

Author(s):: QIAN Chen-xi; XU Jie-chen; ZHANG Lin; YU Zhi-bin; (Department of Aerospace Physiology, Fourth Military Medical University, Xi’an 710032, Shaanxi, China)

关键词:: 单磷酸腺苷活化的蛋白激酶; 心肌; 缺血; 能量代谢; 细胞凋亡

Keywords:: AMP-activated protein kinase; myocardium; ischemia; energy metabolism; apoptosis

分类号:: R333.6

DOI:: -

文献标识码:: A

摘要:: 单磷酸腺苷活化的蛋白激酶(AMP-activated protein kinase，AMPK)广泛存在于心肌细胞中，其是细胞的能量感受器，参与细胞能量代谢调节，在生理和病理情况下都发挥着重要的功能。当细胞发生缺血、缺氧等应激反应时，细胞中三磷酸腺苷(ATP)的浓度降低，AMP的浓度升高，AMP/ATP的比例升高，AMPK被激活。激活的AMPK一方面可抑制ATP的消耗，另一方面刺激细胞产生更多的ATP，使细胞内ATP总量增多，从而可有限地延长细胞内ATP的供应时间，发挥对缺血心肌细胞的保护作用。此外，AMPK激活后可抑制蛋白质合成，可能通过减轻内质网应激以减少缺血引起的心肌细胞凋亡，发挥对心肌的保护作用。

Abstract:: AMP-activated protein kinase (AMPK) serves as a fuel sensor that plays important roles in regulating energy metabolism in cardiomyoctes under both physiological and pathological conditions. AMPK can be activated under such stresses as ischemia or anoxia, which will lead to less ATP, more AMP and increased ratio of AMP to ATP. After activation, AMPK can inhibit ATP utilization, promote ATP production and increase the total amount of ATP in cardiomyocytes. Therefore, AMPK can protect cardiomyocytes by limitedly extending ATP supply time in ischemia. In addition, AMPK can relieve endoplasmic reticulum stress by inhibiting protein synthesis and reduce apoptosis in myocardium.

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AMPK对缺血心肌保护机制的研究进展

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

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