Please use this identifier to cite or link to this item:http://hdl.handle.net/20.500.12105/5405
Novel perspectives on the PHD-HIF oxygen sensing pathway in cardioprotection mediated by IPC and RIPC
Front Physiol. 2015; 6:137
Reperfusion of ischemic cardiac tissue is the standard treatment for improving clinical outcome following myocardial infarction but is inevitably associated with ischemia-reperfusion injury (IRI). Ischemic myocardial injury can be alleviated by exposing the heart to brief episodes of sublethal ischemia-reperfusion prior to the ischemic insult, a phenomenon that has been termed ischemic preconditioning (IPC). Similarly, remote IPC (RIPC) is defined as transient episodes of ischemia at a distant site before a subsequent prolonged injury of the target organ. In this setting, adaptive responses to hypoxia/ischemia in peripheral tissues include the release of soluble factors that have the potential to protect cardiomyocytes remotely. Oxygen fluctuations is a hallmark of insufficient tissue perfusion and ischemic episodes. Emerging evidence indicates that prolyl hydroxylase oxygen sensors (PHDs) and hypoxia-inducible transcription factors (HIFs) are critical regulators of IPC and RIPC. In this review, we discuss recent findings concerning the role of the PHD-HIF axis in IPC and RIPC-mediated cardioprotection and examine molecular pathways and cell types that might be involved. We also appraise the therapeutic value of targeting the PHD-HIF axis to enhance cardiac tolerance against IRI.
Ischemic preconditioning | Heart | PHD oxygen sensors | Hypoxia-inducible factors | Remote ischemic preconditioning | ISCHEMIA-REPERFUSION INJURY | INDUCIBLE FACTOR-I | PRECONDITIONING-INDUCED CARDIOPROTECTION | PERMEABILITY TRANSITION PORE | NITRIC-OXIDE SYNTHASE | INFARCT SIZE | KAPPA-B | METABOLIC SWITCH | COMPLEX-I | RAT-HEART
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