Targeting nucleotide-requiring enzymes: implications for diazoxide-induced cardioprotection.
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The Role of Mitochondrial Reactive Oxygen Species in Cardiovascular Injury and Protective StrategiesPhysiological consequences of complex II inhibition for aging, disease, and the mKATP channelCardioprotective mechanism of diazoxide involves the inhibition of succinate dehydrogenaseThe mitochondrial complex II and ATP-sensitive potassium channel interaction: quantitation of the channel in heart mitochondria.Loss of estrogen receptor beta decreases mitochondrial energetic potential and increases thrombogenicity of platelets in aged female mice.MicroRNA-21 is a key determinant in IL-11/Stat3 anti-apoptotic signalling pathway in preconditioning of skeletal myoblastsDiazoxide potentiates mesenchymal stem cell survival via NF-kappaB-dependent miR-146a expression by targeting FasMitochondrial Channel Opener Diazoxide Attenuates Hypoxia-Induced sFlt-1 Release in Human Choriocarcinoma Cells.Succinate metabolism: a new therapeutic target for myocardial reperfusion injury.The role of mitochondria in protection of the heart by preconditioning.Redox regulation of the mitochondrial K(ATP) channel in cardioprotection.K(ATP) channel therapeutics at the bedside.Role of adenosine A1 and A3 receptors in regulation of cardiomyocyte homeostasis after mitochondrial respiratory chain injury.KATP Channels in the Cardiovascular System.The endogenous mitochondrial complex II inhibitor malonate regulates mitochondrial ATP-sensitive potassium channels: implications for ischemic preconditioning.Inhibition of Succinate Dehydrogenase by Diazoxide Is Independent of the ATP-Sensitive Potassium Channel Subunit Sulfonylurea Type 1 Receptor.Opening of the mitoKATP channel and decoupling of mitochondrial complex II and III contribute to the suppression of myocardial reperfusion hyperoxygenation.Strategies to promote donor cell survival: combining preconditioning approach with stem cell transplantation.Multiplicity of effectors of the cardioprotective agent, diazoxide.Cardioprotection by metabolic shut-down and gradual wake-up.The complex II inhibitor atpenin A5 protects against cardiac ischemia-reperfusion injury via activation of mitochondrial KATP channelsMitochondrial and cell-surface F0F1ATPsynthase in innate and acquired cardioprotection.Inhibitors of succinate: quinone reductase/Complex II regulate production of mitochondrial reactive oxygen species and protect normal cells from ischemic damage but induce specific cancer cell death.Ischemic postconditioning and pinacidil suppress calcium overload in anoxia-reoxygenation cardiomyocytes via down-regulation of the calcium-sensing receptor.Diazoxide-induced respiratory inhibition - a putative mitochondrial K(ATP) channel independent mechanism of pharmacological preconditioning.Genome-Wide Expression Profiling of Anoxia/Reoxygenation in Rat Cardiomyocytes Uncovers the Role of MitoKATP in Energy Homeostasis.The effect of the mitochondrial permeability transition pore on apoptosis in Eimeria tenella host cells.The C. elegans mitochondrial K+(ATP) channel: a potential target for preconditioning.Diazoxide attenuates ischemia/reperfusion injury via upregulation of heme oxygenase-1 after liver transplantation in rats.Variable effects of the mitoK(ATP) channel modulators diazoxide and 5-HD in ATP-depleted renal epithelial cells.Diazoxide preconditioning protects against neuronal cell death by attenuation of oxidative stress upon glutamate stimulation.5-Hydroxydecanoate is metabolised in mitochondria and creates a rate-limiting bottleneck for beta-oxidation of fatty acids.The ATP-sensitive K channel is seizure protective and required for effective dietary therapy in a model of mitochondrial encephalomyopathy.Rapamycin protects testes against germ cell apoptosis and oxidative stress induced by testicular ischemia-reperfusion.Synthesis and Antineoplastic Evaluation of Mitochondrial Complex II (Succinate Dehydrogenase) Inhibitors Derived from Atpenin A5.The mitochondrial K(ATP) channel opener BMS-191095 reduces neuronal damage after transient focal cerebral ischemia in rats.Diazoxide preconditioning of endothelial progenitor cells from streptozotocin-induced type 1 diabetic rats improves their ability to repair diabetic cardiomyopathy.
P2860
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P2860
Targeting nucleotide-requiring enzymes: implications for diazoxide-induced cardioprotection.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh-hant
name
Targeting nucleotide-requiring ...... xide-induced cardioprotection.
@en
Targeting nucleotide-requiring ...... xide-induced cardioprotection.
@nl
type
label
Targeting nucleotide-requiring ...... xide-induced cardioprotection.
@en
Targeting nucleotide-requiring ...... xide-induced cardioprotection.
@nl
prefLabel
Targeting nucleotide-requiring ...... xide-induced cardioprotection.
@en
Targeting nucleotide-requiring ...... xide-induced cardioprotection.
@nl
P2093
P2860
P1476
Targeting nucleotide-requiring ...... xide-induced cardioprotection.
@en
P2093
Andre Terzic
Arturo Valverde
Cevher Ozcan
David G L Van Wylen
Peter Bast
Petras P Dzeja
P2860
P304
P356
10.1152/AJPHEART.00847.2002
P577
2003-04-01T00:00:00Z