Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/5405
Título
Novel perspectives on the PHD-HIF oxygen sensing pathway in
cardioprotection mediated by IPC and RIPC
Autor(es)
Fecha de publicación
2015
Cita
Front Physiol. 2015; 6:137
Idioma
Inglés
Tipo de documento
journal article
Resumen
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.
Palabras clave
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
Versión en línea
DOI
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