Cardiac myocyte-specific expression of inducible nitric oxide synthase protects against ischemia/reperfusion injury by preventing mitochondrial permeability transition.
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Oxidative-Nitrosative Stress and Myocardial Dysfunctions in Sepsis: Evidence from the Literature and Postmortem ObservationsNitric oxide synthases in heart failureTargeting Nitric Oxide with Natural Derived Compounds as a Therapeutic Strategy in Vascular DiseasesProtein S-nitrosylation and cardioprotectionThe valosin-containing protein is a novel mediator of mitochondrial respiration and cell survival in the heart in vivo.Inhibition of inducible nitric oxide synthase prevents mitochondrial damage and improves survival of steatotic partial liver grafts.Comprehensive measurement of respiratory activity in permeabilized cells using extracellular flux analysisTherapeutic hypothermia cardioprotection via Akt- and nitric oxide-mediated attenuation of mitochondrial oxidants.Postischemic deactivation of cardiac aldose reductase: role of glutathione S-transferase P and glutaredoxin in regeneration of reduced thiols from sulfenic acidseNOS is required for acute in vivo ischemic preconditioning of the heart: effects of ischemic duration and sex.Adjuvant cardioprotection in cardiac surgery: update.Regulation of mitochondrial processes by protein S-nitrosylation.Darbepoetin-mediated cardioprotection after myocardial infarction involves multiple mechanisms independent of erythropoietin receptor-common beta-chain heteroreceptor.Netrin-1 improves post-injury cardiac function in vivo via DCC/NO-dependent preservation of mitochondrial integrity, while attenuating autophagy.Animal models of cardiovascular diseasesNetrin-1 abrogates ischemia/reperfusion-induced cardiac mitochondrial dysfunction via nitric oxide-dependent attenuation of NOX4 activation and recoupling of NOS.Reactive oxygen species in cardiovascular disease.Isoflurane postconditioning protects against reperfusion injury by preventing mitochondrial permeability transition by an endothelial nitric oxide synthase-dependent mechanismProtein S-glutathiolation: redox-sensitive regulation of protein function.Altered expression of mitochondrial electron transport chain proteins and improved myocardial energetic state during late ischemic preconditioning.Role of inducible nitric oxide synthase in mitochondrial depolarization and graft injury after transplantation of fatty liversWhat makes the mitochondria a killer? Can we condition them to be less destructive?The COX-2/PGI2 receptor axis plays an obligatory role in mediating the cardioprotection conferred by the late phase of ischemic preconditioning.Redox mechanisms of cardiomyocyte mitochondrial protection.Cardiomyocyte-restricted overexpression of extracellular superoxide dismutase increases nitric oxide bioavailability and reduces infarct size after ischemia/reperfusion.Roles of the nitric oxide signaling pathway in cardiac ischemic preconditioning against myocardial ischemia-reperfusion injury.Later phase cardioprotection of ischemic post-conditioning against ischemia/reperfusion injury depends on iNOS and PI3K-Akt pathway.Roles of endothelial nitric oxide synthase (eNOS) and mitochondrial permeability transition pore (MPTP) in epoxyeicosatrienoic acid (EET)-induced cardioprotection against infarction in intact rat hearts.Genetic Deficiency of Glutathione S-Transferase P Increases Myocardial Sensitivity to Ischemia-Reperfusion Injury.Loss of cardioprotection with ageing.Sulindac confers high level ischemic protection to the heart through late preconditioning mechanisms.Bench-to-bedside review: nitric oxide in critical illness--update 2008.Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical Issue for Clinicians and Forensic Pathologists.Usefulness of combining intermittent hypoxia and physical exercise in the treatment of obesity.Rodent models of heart failure: an updated review.Molecular mechanisms of ischemic conditioning: translation into patient outcomes.Trans-system mechanisms against ischemic myocardial injury.Repeated ischaemic preconditioning: a novel therapeutic intervention and potential underlying mechanisms.Toll-like receptor 7/8 agonist resiquimod induces late preconditioning in neonatal cardiac myocytes.Environmental Determinants of Cardiovascular Disease.
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P2860
Cardiac myocyte-specific expression of inducible nitric oxide synthase protects against ischemia/reperfusion injury by preventing mitochondrial permeability transition.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
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artigo científico
@pt
bilimsel makale
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scientific article published on 20 October 2008
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Cardiac myocyte-specific expre ...... drial permeability transition.
@en
Cardiac myocyte-specific expre ...... drial permeability transition.
@nl
type
label
Cardiac myocyte-specific expre ...... drial permeability transition.
@en
Cardiac myocyte-specific expre ...... drial permeability transition.
@nl
prefLabel
Cardiac myocyte-specific expre ...... drial permeability transition.
@en
Cardiac myocyte-specific expre ...... drial permeability transition.
@nl
P2093
P2860
P1433
P1476
Cardiac myocyte-specific expre ...... drial permeability transition.
@en
P2093
Aruni Bhatnagar
Daniel J Conklin
Detlef Obal
Gregg Rokosh
Jay L Zweier
Jürgen Schrader
Matthew B West
Murugesan Velayutham
Rachel J Keith
Roberto Bolli
P2860
P304
P356
10.1161/CIRCULATIONAHA.108.791533
P407
P577
2008-10-20T00:00:00Z