Division of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, 55 Lake Avenue N, S3-855, Worcester, MA 01655, USA.
Curr Opin Pharmacol. 2010 Apr;10(2):111-5. doi: 10.1016/j.coph.2009.11.009. Epub 2010 Jan 8.
AMP-activated protein kinase (AMPK) was initially viewed as energy sensor and activated by increased intracellular concentrations of AMP following nutrient deprivation. Physiological or pathological stimuli that deplete cellular energy activate AMPK that coordinates a cellular program that limits further ATP depletion and promotes compensatory changes that maintain cellular ATP levels. Recent studies revealed novel roles of AMPK independent of energy status, thereby increasing our understanding of multi-functional roles of AMPK in cells important in pathogenesis of cardiovascular diseases. This enzyme represents an attractive therapeutic target for vascular disease treatment in the future.
腺苷酸活化蛋白激酶（AMPK）最初被视为能量传感器，在营养物质匮乏时，细胞内 AMP 浓度增加会激活 AMPK。生理或病理刺激会消耗细胞能量，激活 AMPK，协调细胞程序，限制进一步的 ATP 消耗，并促进代偿性变化，以维持细胞内 ATP 水平。最近的研究揭示了 AMPK 独立于能量状态的新作用，从而增加了我们对其在心血管疾病发病机制中重要的细胞中的多功能作用的理解。这种酶代表了未来治疗血管疾病的一个有吸引力的治疗靶点。
