2026-06-14T03:37:38Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/54052024-09-27T09:52:12Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Martin-Puig, Silvia author Tello, Daniel author Aragones, Julian author 2015 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. Front Physiol. 2015; 6:137 10.3389/fphys.2015.00137 1664-042X Frontiers in Physiology 26042040 http://hdl.handle.net/20.500.12105/5405 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