2026-06-14T05:05:41Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/54052024-09-27T09:52:12Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Martin-Puig, Silvia
author
Tello, Daniel
author
Aragones, Julian
funder
Ministerio de Economía y Competitividad (España)
funder
Comunidad de Madrid (España)
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
funder
Red de Investigación Cardiovascular (RIC) (España)
2017-11-27T13:49:52Z
2017-11-27T13:49:52Z
2015
Front Physiol. 2015; 6:137
10.3389/fphys.2015.00137
1664-042X
Frontiers in Physiology
26042040
http://hdl.handle.net/20.500.12105/5405
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.
eng
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
Novel perspectives on the PHD-HIF oxygen sensing pathway in
cardioprotection mediated by IPC and RIPC
journal article
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