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A new sense of protection: role of the Ca2+-sensing receptor in ischemic preconditioning.

机译:一种新的保护感:Ca2 +感应受体在缺血预处理中的作用。

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摘要

the phenomenon of ischemic preconditioning (IPC), a condition in which brief periods of ischemia increase the tolerance of the heart to subsequent ischemic injury, is of immense clinical interest. Many signaling pathways are implicated in the induction of IPC; however, the initiation of the response involves activation of G protein-coupled receptors (GPCRs) and their downstream effectors (e.g., a variety of prosurvival kinase cascades) that ultimately converge to inhibit the opening of the mitochondrial permeability transition pore and limit subsequent proapoptotic activity (2, 4).
机译:缺血预适应(IPC)现象(短暂的局部缺血会增加心脏对随后的局部缺血性损伤的耐受性的一种疾病)具有巨大的临床意义。 IPC的诱导涉及许多信号传导途径。然而,响应的启动涉及激活G蛋白偶联受体(GPCR)及其下游效应物(例如,各种生存激酶级联反应),这些作用最终收敛以抑制线粒体通透性过渡孔的开放并限制随后的促凋亡活性(2,4)。

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