Impact of hypoglycemic agents on myocardial ischemic preconditioning
Impact of hypoglycemic agents on myocardial ischemic preconditioning
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DOI：
10.4239/wjd.v5.i3.258
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发表时间：
2014-06-15
影响因子：
4.2
通讯作者：
Hueb, Whady
中科院分区：
文献类型：
--
作者：
Garcia, Rosa Maria Rahmi;Rezende, Paulo Cury;Hueb, Whady
Murry等在1986年发现了深度保护的内在机制，称为缺血预适应。这种现象背后的复杂细胞信号级联仍然存在争议，只有部分理解。然而，有证据表明，腺苷，在最初的缺血损伤期间释放，激活各种G蛋白偶联激动剂，如阿片类药物，缓激肽，和儿茶酚胺，导致蛋白激酶的激活，特别是蛋白激酶C（PKC）。这导致PKC从细胞质易位到肌膜，在那里它刺激ATP敏感性K+通道的开放，这赋予对缺血的抵抗力。众所周知，一系列不同的降糖药在不同的细胞水平上激活相同的信号级联，可以干扰缺血预处理的保护作用。本文综述了几种降糖药物对心肌缺血预适应的影响。
Murry et al in 1986 discovered the intrinsic mechanism of profound protection called ischemic preconditioning. The complex cellular signaling cascades underlying this phenomenon remain controversial and are only partially understood. However, evidence suggests that adenosine, released during the initial ischemic insult, activates a variety of G protein-coupled agonists, such as opioids, bradykinin, and catecholamines, resulting in the activation of protein kinases, especially protein kinase C (PKC). This leads to the translocation of PKC from the cytoplasm to the sarcolemma, where it stimulates the opening of the ATP-sensitive K+ channel, which confers resistance to ischemia. It is known that a range of different hypoglycemic agents that activate the same signaling cascades at various cellular levels can interfere with protection from ischemic preconditioning. This review examines the effects of several hypoglycemic agents on myocardial ischemic preconditioning in animal studies and clinical trials.