Biophysical properties and functional consequences of reactive oxygen species (ROS)-induced ROS release in intact myocardium.
about
Mitochondrial network energetics in the heart.Potential implication of the chemical properties and bioactivity of nitrone spin traps for therapeuticsImpaired mitochondrial network excitability in failing guinea-pig cardiomyocytesFunctional crosstalk between the mitochondrial PTP and KATP channels determine arrhythmic vulnerability to oxidative stressMitochondrial reactive oxygen species (ROS) and ROS-induced ROS release.Mitochondrial ion channels/transporters as sensors and regulators of cellular redox signaling.Pathophysiological mechanisms of catecholamine and cocaine-mediated cardiotoxicity.Role of NADPH oxidase and xanthine oxidase in mediating inducible VT/VF and triggered activity in a canine model of myocardial ischemiaInhibition of NAPDH Oxidase 2 (NOX2) Prevents Oxidative Stress and Mitochondrial Abnormalities Caused by Saturated Fat in Cardiomyocytes.Glutathione/thioredoxin systems modulate mitochondrial H2O2 emission: an experimental-computational study.The continuing evolution of the Langendorff and ejecting murine heart: new advances in cardiac phenotyping.Reperfusion injury and reactive oxygen species: The evolution of a concept.Oxidative stress generated during monensin treatment contributes to altered Toxoplasma gondii mitochondrial function.Glutathione oxidation unmasks proarrhythmic vulnerability of chronically hyperglycemic guinea pigsMitochondrial targets for arrhythmia suppression: is there a role for pharmacological intervention?Mitochondrial channels: ion fluxes and more.The mitochondrial translocator protein and arrhythmogenesis in ischemic heart diseaseSynchronism in mitochondrial ROS flashes, membrane depolarization and calcium sparks in human carcinoma cells.Antioxidant therapy for atrial fibrillation: what is the next step?Involvement of reactive oxygen species derived from mitochondria in neuronal injury elicited by methylmercury.The role of succinate and ROS in reperfusion injury - A critical appraisal.Reducing mitochondrial bound hexokinase II mediates transition from non-injurious into injurious ischemia/reperfusion of the intact heart.Inhibition of NADPH oxidase 2 (NOX2) prevents sepsis-induced cardiomyopathy by improving calcium handling and mitochondrial function.Functional Role of Mitochondria in Arrhythmogenesis.Ultrafine Particulate Matter Increases Cardiac Ischemia/Reperfusion Injury via Mitochondrial Permeability Transition Pore.The Mitochondrial Translocator Protein and the Emerging Link Between Oxidative Stress and Arrhythmias in the Diabetic Heart
P2860
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P2860
Biophysical properties and functional consequences of reactive oxygen species (ROS)-induced ROS release in intact myocardium.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年学术文章
@wuu
2011年学术文章
@zh
2011年学术文章
@zh-cn
2011年学术文章
@zh-hans
2011年学术文章
@zh-my
2011年学术文章
@zh-sg
2011年學術文章
@yue
2011年學術文章
@zh-hant
name
Biophysical properties and fun ...... release in intact myocardium.
@en
Biophysical properties and functional consequences of reactive oxygen species
@nl
type
label
Biophysical properties and fun ...... release in intact myocardium.
@en
Biophysical properties and functional consequences of reactive oxygen species
@nl
prefLabel
Biophysical properties and fun ...... release in intact myocardium.
@en
Biophysical properties and functional consequences of reactive oxygen species
@nl
P2093
P2860
P1476
Biophysical properties and fun ...... release in intact myocardium.
@en
P2093
Chaoqin Xie
Fadi G Akar
Justin Kauffman
Nora Biary
P2860
P304
P356
10.1113/JPHYSIOL.2011.214239
P407
P577
2011-08-08T00:00:00Z