AMPK mediates autophagy during myocardial ischemia in vivo
AMPK mediates autophagy during myocardial ischemia in vivo
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DOI：
10.4161/auto.4281
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发表时间：
2007-07-01
期刊：
影响因子：
13.3
通讯作者：
Sadoshima, Junichi
中科院分区：
文献类型：
--
作者：
Takagi, Hiromitsu;Matsui, Yutaka;Sadoshima, Junichi
我们最近表明，在体小鼠心脏中，自噬由缺血和再灌注诱导。缺血通过一种依赖AMP活化蛋白激酶（AMPK）的机制刺激自噬，而缺血后的再灌注则通过一种依赖Beclin 1但不依赖AMPK的机制刺激自噬。自噬在缺血和再灌注过程中发挥着不同的作用：自噬在缺血期间可能具有保护作用，而在再灌注期间可能有害。我们将讨论AMPK在体内心肌缺血期间介导自噬的作用。
We have recently shown that autophagy is induced by ischemia and reperfusion in the mouse heart in vivo. Ischemia stimulates autophagy through an AMP activated protein kinase (AMPK)-dependent mechanism whereas reperfusion after ischemia stimulates autophagy through a Beclin 1-dependent, but AMPK-independent, mechanism. Autophagy plays distinct roles during ischemia and reperfusion: autophagy may be protective during ischemia, whereas it may be detrimental during reperfusion. We will discuss the role of AMPK in mediating autophagy during myocardial ischemia in vivo.