Oxidant stress during simulated ischemia primes cardiomyocytes for cell death during reperfusion. - Wikidata - wikimedia - TriplyDB

Oxidant stress during simulated ischemia primes cardiomyocytes for cell death during reperfusion.

Oxidant stress during simulated ischemia primes cardiomyocytes for cell death during reperfusion.

http://www.wikidata.org/entity/Q50684490

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Lung cell hypoxia: role of mitochondrial reactive oxygen species signaling in triggering responses Role of the MPTP in conditioning the heart - translatability and mechanism Reactive Oxygen Species: A Key Hallmark of Cardiovascular Disease The role of oxidized cytochrome c in regulating mitochondrial reactive oxygen species production and its perturbation in ischaemia Hexokinase II knockdown results in exaggerated cardiac hypertrophy via increased ROS production Silencing of cardiac mitochondrial NHE1 prevents mitochondrial permeability transition pore opening.The targeting of cyclophilin D by RNAi as a novel cardioprotective therapy: evidence from two-photon imaging.The protective effects of Polygonum multiflorum stilbeneglycoside preconditioning in an ischemia/reperfusion model of HUVECs Glycolytic oscillations in single ischemic cardiomyocytes at near anoxia.Potential phytoestrogen alternatives exert cardio-protective mechanisms via estrogen receptors PGC-1α attenuates hydrogen peroxide-induced apoptotic cell death by upregulating Nrf-2 via GSK3β inactivation mediated by activated p38 in HK-2 Cells.Reactive oxygen species and redox compartmentalization Lipocalin-type prostaglandin D synthase protects against oxidative stress-induced neuronal cell death.The molecular biology and pathophysiology of vascular calcification.Redox signaling in cardiac myocytes.Lipocalin-2 as mediator of chemokine expression and granulocyte infiltration during ischemia and reperfusion.Ischemia/reperfusion injury and cardioprotective mechanisms: Role of mitochondria and reactive oxygen species Distinct mPTP activation mechanisms in ischaemia-reperfusion: contributions of Ca2+, ROS, pH, and inorganic polyphosphate.Oxidation of Akt2 kinase promotes cell migration and regulates G1-S transition in the cell cycle.Activation of Chymotrypsin-Like Activity of the Proteasome during Ischemia Induces Myocardial Dysfunction and Death Protective role of adiponectin in a rat model of intestinal ischemia reperfusion injury Ursolic-Acid-Enriched Herba Cynomorii Extract Protects against Oxidant Injury in H9c2 Cells and Rat Myocardium by Increasing Mitochondrial ATP Generation Capacity and Enhancing Cellular Glutathione Redox Cycling, Possibly through Mitochondrial Uncou Metallothionein alleviates oxidative stress-induced endoplasmic reticulum stress and myocardial dysfunction.Effect of taurine on ischemia-reperfusion injury.Lung oxidative damage by hypoxia Pharmacological approaches to the treatment of oxidative stress-induced cardiovascular dysfunctions.Oxygen therapy in acute coronary syndrome: are the benefits worth the risk?Visualization of the spatial and temporal dynamics of MAPK signaling using fluorescence imaging techniques.Hypoxia triggers AMPK activation through reactive oxygen species-mediated activation of calcium release-activated calcium channels.Chronology of mitochondrial and cellular events during skeletal muscle ischemia-reperfusion.Genetically encoded fluorescent redox probes.A novel pathway of NADPH oxidase/vascular peroxidase 1 in mediating oxidative injury following ischemia-reperfusion.Mitochondrial NHE1: a newly identified target to prevent heart disease.Mechanism of glutathione depletion during simulated ischemia-reperfusion of H9c2 cardiac myocytes.ROS-mediated PARP activity undermines mitochondrial function after permeability transition pore opening during myocardial ischemia-reperfusion Primary bovine skeletal muscle cells enters apoptosis rapidly via the intrinsic pathway when available oxygen is removed.Mitochondrial oxidant stress triggers cell death in simulated ischemia-reperfusion.Reactive oxygen species production in energized cardiac mitochondria during hypoxia/reoxygenation: modulation by nitric oxide.Reversible oxidation of mitochondrial peroxiredoxin 3 in mouse heart subjected to ischemia and reperfusion.Mechanism underlying methyl eugenol attenuation of intestinal ischemia/reperfusion injury.

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P2860

Oxidant stress during simulated ischemia primes cardiomyocytes for cell death during reperfusion.

http://www.wikidata.org/entity/Q50684490

description

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Oxidant stress during simulate ...... cell death during reperfusion.

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Oxidant stress during simulate ...... cell death during reperfusion.

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Oxidant stress during simulate ...... cell death during reperfusion

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Emmanuel Robin

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Gabriel Loor

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Gregory B Waypa

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Hirotaro Iwase

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Jeremy D Marks

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Paul T Schumacker

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Terry L Vanden Hoek

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P2860

Reducing the environmental sensitivity of yellow fluorescent protein. Mechanism and applications

Investigating mitochondrial redox potential with redox-sensitive green fluorescent protein indicators

Myocardial reperfusion: a double-edged sword?

Complex III releases superoxide to both sides of the inner mitochondrial membrane

Increased myocardial dysfunction after ischemia-reperfusion in mice lacking glucose-6-phosphate dehydrogenase

Mitochondrial complex III is required for hypoxia-induced ROS production and cellular oxygen sensing

Chaperone activity with a redox switch.

Detection and characterization of the product of hydroethidine and intracellular superoxide by HPLC and limitations of fluorescence

Methods of detection of vascular reactive species: nitric oxide, superoxide, hydrogen peroxide, and peroxynitrite.

Direct measurement of free radical generation following reperfusion of ischemic myocardium

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