Mechanism of cardioprotection by early ischemic preconditioning.
Mechanism of cardioprotection by early ischemic preconditioning.
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DOI：
10.1007/s10557-010-6236-x
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发表时间：
2010-06
影响因子：
3.4
通讯作者：
Downey JM
中科院分区：
文献类型：
--
作者：
Yang X;Cohen MV;Downey JM
A series of brief ischemia/reperfusion cycles (termed ischemic preconditioning, IPC) limits myocardial injury produced by a subsequent prolonged period of coronary artery occlusion and reperfusion. Over the last 2 decades our understanding of IPC’s mechanism has increased exponentially. Hearts exposed to IPC have a better metabolic and ionic status during prolonged ischemia compared to naïve hearts. However, this difference is not thought to be the main mechanism by which IPC protects against infarction. Signaling pathways that are activated by IPC distinguish IPC hearts from naïve hearts. During the trigger phase of IPC, adenosine, bradykinin and opioid receptors are occupied. Although these three receptors trigger signaling through divergent pathways, the signaling converges on protein kinase C. We have proposed that at the end of the index ischemia the activated PKC sensitizes the low-affinity A2b adenosine receptor (A2bAR) through phosphorylation of either the receptor or its coupling proteins so that A2bAR can be activated by endogenous adenosine released by the previously ischemic cardiomyocytes. The sensitized A2bAR would then be responsible for activation of the survival kinases including PI3 kinase, Akt and ERK which then act to inhibit lethal mitochondrial permeability transition pore formation which normally uncouples mitochondria and destroys many myocytes in the first minutes of reperfusion. Herein we review the evidence for the above mechanisms and their functional details.
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影响因子：
9.5
作者：
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通讯作者：
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影响因子：
20.1
作者：
BANERJEE, A;LOCKEWINTER, C;HARKEN, AH
通讯作者：
HARKEN, AH
影响因子：
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作者：
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通讯作者：
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影响因子：
37.8
作者：
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通讯作者：
Semenza, GL
DOI：
10.1073/pnas.191369098
发表时间：
2001-09-25
影响因子：
11.1
作者：
Chen, L;Hahn, H;Mochly-Rosen, D
通讯作者：
Mochly-Rosen, D