Redox signaling at reperfusion is required for protection from ischemic preconditioning but not from a direct PKC activator. - Wikidata - wikimedia - TriplyDB

Redox signaling at reperfusion is required for protection from ischemic preconditioning but not from a direct PKC activator.

Redox signaling at reperfusion is required for protection from ischemic preconditioning but not from a direct PKC activator.

http://www.wikidata.org/entity/Q37138742

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Protein Oxidative Modifications: Beneficial Roles in Disease and Health The reno-vascular A2B adenosine receptor protects the kidney from ischemia Concentration-dependent wrestling between detrimental and protective effects of H2O2 during myocardial ischemia/reperfusion No impact of protein phosphatases on connexin 43 phosphorylation in ischemic preconditioning.Cardioprotective PKG-independent NO signaling at reperfusion Redox signaling pathways involved in neuronal ischemic preconditioning Infarct limitation by a protein kinase G activator at reperfusion in rabbit hearts is dependent on sensitizing the heart to A2b agonists by protein kinase C Injection of isolated mitochondria during early reperfusion for cardioprotection.Mitochondrial therapeutics for cardioprotection.Protection of peroxiredoxin II on oxidative stress-induced cardiomyocyte death and apoptosis.Mitochondrial reactive oxygen species: which ROS signals cardioprotection?Regulation and pharmacology of the mitochondrial permeability transition pore.To prevent, protect and save the ischemic heart: antioxidants revisited.Mechanism of cardioprotection by early ischemic preconditioning Redox balance and cardioprotection.The "Goldilocks Zone" from a redox perspective-Adaptive vs. deleterious responses to oxidative stress in striated muscle.The Protective Role of the TOPK/PBK Pathway in Myocardial Ischemia/Reperfusion and H₂O₂-Induced Injury in H9C2 Cardiomyocytes.Catestatin reduces myocardial ischaemia/reperfusion injury: involvement of PI3K/Akt, PKCs, mitochondrial KATP channels and ROS signalling.Lack of Contribution of p66shc and Its Mitochondrial Translocation to Ischemia-Reperfusion Injury and Cardioprotection by Ischemic Preconditioning.Dehydroascorbic acid as pre-conditioner: protection from lipopolysaccharide induced mitochondrial damage.Participation of protein kinase C in the activation of Nrf2 signaling by ischemic preconditioning in the isolated rabbit heart.Redox-dependent increases in glutathione reductase and exercise preconditioning: role of NADPH oxidase and mitochondria.What is the optimal postconditioning algorithm?

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P2860

Redox signaling at reperfusion is required for protection from ischemic preconditioning but not from a direct PKC activator.

http://www.wikidata.org/entity/Q37138742

description

2007 nî lūn-bûn

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2007年の論文

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年學術文章

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2007年學術文章

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2007年學術文章

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name

Redox signaling at reperfusion ...... t from a direct PKC activator.

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Redox signaling at reperfusion ...... t from a direct PKC activator.

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type

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Redox signaling at reperfusion ...... t from a direct PKC activator.

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Redox signaling at reperfusion ...... t from a direct PKC activator.

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Redox signaling at reperfusion ...... t from a direct PKC activator.

@en

Redox signaling at reperfusion ...... t from a direct PKC activator.

@nl

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Basic Research in Cardiology

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Redox signaling at reperfusion ...... t from a direct PKC activator.

@en

P2093

Dimitrios T Kremastinos

http://www.w3.org/2001/XMLSchema#string

Efstathios K Iliodromitis

http://www.w3.org/2001/XMLSchema#string

James M Downey

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Michael V Cohen

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Turhan Dost

http://www.w3.org/2001/XMLSchema#string

Xi-Ming Yang

http://www.w3.org/2001/XMLSchema#string

Yanping Liu

http://www.w3.org/2001/XMLSchema#string

P2860

Preconditioning protects by inhibiting the mitochondrial permeability transition.

Glycogen synthase kinase-3beta mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore

Postconditioning protects rabbit hearts through a protein kinase C-adenosine A2b receptor cascade.

GSK3beta inhibition and K(ATP) channel opening mediate acute opioid-induced cardioprotection at reperfusion.

Cardioprotection and mitochondrial S-nitrosation: effects of S-nitroso-2-mercaptopropionyl glycine (SNO-MPG) in cardiac ischemia-reperfusion injury

Protein kinase C protects preconditioned rabbit hearts by increasing sensitivity of adenosine A2b-dependent signaling during early reperfusion

Mechanism of myocardial "stunning".

Zinc release from protein kinase C as the common event during activation by lipid second messenger or reactive oxygen.

Marked reduction of free radical generation and contractile dysfunction by antioxidant therapy begun at the time of reperfusion. Evidence that myocardial "stunning" is a manifestation of reperfusion injury.

Opening of ATP-sensitive potassium channels causes generation of free radicals in vascular smooth muscle cells.

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10.1007/S00395-007-0683-Y

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