Cohen M V, Downey J M
Department of Physiology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA.
Br J Pharmacol. 2007 Nov;152(6):833-4. doi: 10.1038/sj.bjp.0707453. Epub 2007 Sep 17.
Classical ischaemic preconditioning, delayed or second window preconditioning and postconditioning are forms of cardioprotection that are dependent on cell surface receptors, intracellular signalling molecules and kinases that ultimately block formation of the mitochondrial permeability transition. The latter is presumed to cause myocardial necrosis as well as apoptosis, so prevention of its formation upon resumption of perfusion after a prolonged coronary occlusion should be cardioprotective. In all of these forms of cardioprotection, formation of cGMP and activation of protein kinase G (PKG) are recognized to be key steps in the signal transduction pathway. Burley et al. highlight the roles of cGMP and PKG in their comprehensive review. They describe the basic biology of PKG and emphasize its compartmentalization, which may be responsible for the frustration induced by assays for PKG in whole cell lysates and for the spurious conclusions about the role of PKG in cardioprotection. This review will be useful to both the novice and the seasoned investigator.
经典缺血预处理、延迟或第二窗预处理以及后处理是几种心脏保护形式，它们依赖于细胞表面受体、细胞内信号分子和激酶，这些最终会阻止线粒体通透性转换的形成。后者被认为会导致心肌坏死以及细胞凋亡，因此在长时间冠状动脉闭塞后恢复灌注时防止其形成应该具有心脏保护作用。在所有这些心脏保护形式中，cGMP的形成和蛋白激酶G（PKG）的激活被认为是信号转导途径中的关键步骤。伯利等人在他们的全面综述中强调了cGMP和PKG的作用。他们描述了PKG的基本生物学特性，并强调了其区室化，这可能是全细胞裂解物中PKG检测所导致的矛盾结果以及关于PKG在心脏保护中作用的错误结论的原因。这篇综述对新手和经验丰富的研究人员都将有所帮助。
