Inhibited mitochondrial respiration by amobarbital during cardiac ischaemia improves redox state and reduces matrix Ca2+ overload and ROS release. - Wikidata - awgldk - TriplyDB

Inhibited mitochondrial respiration by amobarbital during cardiac ischaemia improves redox state and reduces matrix Ca2+ overload and ROS release.

Inhibited mitochondrial respiration by amobarbital during cardiac ischaemia improves redox state and reduces matrix Ca2+ overload and ROS release.

http://www.wikidata.org/entity/Q46972249

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The Role of Mitochondrial Functional Proteins in ROS Production in Ischemic Heart Diseases Mitochondrial reactive oxygen species: a double edged sword in ischemia/reperfusion vs preconditioning Anaesthetics as cardioprotectants: translatability and mechanism Cardiolipin as an oxidative target in cardiac mitochondria in the aged rat Electron flow into cytochrome c coupled with reactive oxygen species from the electron transport chain converts cytochrome c to a cardiolipin peroxidase: role during ischemia-reperfusion Cytoprotection by the modulation of mitochondrial electron transport chain: the emerging role of mitochondrial STAT3 Mitochondrial reactive oxygen species production in excitable cells: modulators of mitochondrial and cell function.Mitochondrial VDAC1: A Key Gatekeeper as Potential Therapeutic Target Isoflurane modulates cardiac mitochondrial bioenergetics by selectively attenuating respiratory complexes Mitochondria in the elderly: Is acetylcarnitine a rejuvenator?Potential therapeutic benefits of strategies directed to mitochondria.Mitochondrial targets for volatile anesthetics against cardiac ischemia-reperfusion injury Reversible blockade of complex I or inhibition of PKCβ reduces activation and mitochondria translocation of p66Shc to preserve cardiac function after ischemia Blockade of electron transport during ischemia preserves bcl-2 and inhibits opening of the mitochondrial permeability transition pore Mitochondrial approaches to protect against cardiac ischemia and reperfusion injury.Reduction of infarct size by the therapeutic protein TAT-Ndi1 in vivo Ischemia/reperfusion injury and cardioprotective mechanisms: Role of mitochondria and reactive oxygen species Differential effects of buffer pH on Ca(2+)-induced ROS emission with inhibited mitochondrial complexes I and III.Adding ROS quenchers to cold K+ cardioplegia reduces superoxide emission during 2-hour global cold cardiac ischemia.Isoflurane anesthesia initiated at the onset of reperfusion attenuates oxidative and hypoxic-ischemic brain injury Ranolazine reduces Ca2+ overload and oxidative stress and improves mitochondrial integrity to protect against ischemia reperfusion injury in isolated hearts Measuring mitochondrial function in intact cardiac myocytes.Valeriana officinalis Extracts Ameliorate Neuronal Damage by Suppressing Lipid Peroxidation in the Gerbil Hippocampus Following Transient Cerebral Ischemia Damage to mitochondrial complex I during cardiac ischemia reperfusion injury is reduced indirectly by anti-anginal drug ranolazine.Enhanced charge-independent mitochondrial free Ca(2+) and attenuated ADP-induced NADH oxidation by isoflurane: Implications for cardioprotection Blockade of electron transport at the onset of reperfusion decreases cardiac injury in aged hearts by protecting the inner mitochondrial membrane.Blockade of electron transport before ischemia protects mitochondria and decreases myocardial injury during reperfusion in aged rat hearts Pim-1 Kinase Regulating Dynamics Related Protein 1 Mediates Sevoflurane Postconditioning-induced Cardioprotection.Mitochondrial handling of excess Ca2+ is substrate-dependent with implications for reactive oxygen species generation.Enhanced Na+/H+ exchange during ischemia and reperfusion impairs mitochondrial bioenergetics and myocardial function Modulation of mitochondrial bioenergetics in the isolated Guinea pig beating heart by potassium and lidocaine cardioplegia: implications for cardioprotection.Safety and Efficacy of Ranolazine for the Treatment of Chronic Angina Pectoris.Mitochondria as metabolizers and targets of nitrite.Metabolic fingerprint of ischaemic cardioprotection: importance of the malate-aspartate shuttle.Miltirone exhibits antileukemic activity by ROS-mediated endoplasmic reticulum stress and mitochondrial dysfunction pathways.The role of succinate and ROS in reperfusion injury - A critical appraisal.Optical Cryoimaging Reveals a Heterogeneous Distribution of Mitochondrial Redox State in ex vivo Guinea Pig Hearts and Its Alteration During Ischemia and Reperfusion.Reactive oxygen species production induced by pore opening in cardiac mitochondria: The role of complex III.Reactive oxygen species production induced by pore opening in cardiac mitochondria: The role of complex II.Inhibition of mitochondrial complex I improves glucose metabolism independently of AMPK activation.

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Inhibited mitochondrial respiration by amobarbital during cardiac ischaemia improves redox state and reduces matrix Ca2+ overload and ROS release.

http://www.wikidata.org/entity/Q46972249

description

2008 nî lūn-bûn

@nan

2008年の論文

@ja

2008年学术文章

@wuu

2008年学术文章

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2008年学术文章

@zh-cn

2008年学术文章

@zh-hans

2008年学术文章

@zh-my

2008年学术文章

@zh-sg

2008年學術文章

@yue

2008年學術文章

@zh-hant

name

Inhibited mitochondrial respir ...... Ca2+ overload and ROS release.

@en

Inhibited mitochondrial respir ...... Ca2+ overload and ROS release.

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type

label

Inhibited mitochondrial respir ...... Ca2+ overload and ROS release.

@en

Inhibited mitochondrial respir ...... Ca2+ overload and ROS release.

@nl

prefLabel

Inhibited mitochondrial respir ...... Ca2+ overload and ROS release.

@en

Inhibited mitochondrial respir ...... Ca2+ overload and ROS release.

@nl

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J.CARDIORES.2007.08.008

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Cardiovascular Research

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Inhibited mitochondrial respir ...... Ca2+ overload and ROS release.

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Amadou K S Camara

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David F Stowe

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Edward J Lesnefsky

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Mohammed Aldakkak

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Qun Chen

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406-415

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scholarly article

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10.1016/J.CARDIORES.2007.08.008

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2

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77

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2008-01-01T00:00:00Z

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5943323

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17900548

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