cGMP signalling in pre- and post-conditioning: the role of mitochondria.

No abstract is available for this paper.

• Publication year

  2008

• Venue

  Cardiovascular Research

• Publication date

  Unknown publication date

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1093/CVR/CVM050PMID 18006449
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Endothelial Nitric Oxide Synthase Plays an Obligatory Role in the Late Phase of Ischemic Preconditioning by Activating the Protein Kinase C&egr;–p44/42 Mitogen-Activated Protein Kinase–pSer-Signal Transducers and Activators of Transcription1/3 Pathway

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• The mitochondrial permeability transition from in vitro artifact to disease target

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• Post–conditioning induced cardioprotection requires signaling through a redox–sensitive mechanism, mitochondrial ATP–sensitive K+ channel and protein kinase C activation

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• Nitric oxide is a preconditioning mimetic and cardioprotectant and is the basis of many available infarct-sparing strategies.

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• Opioid-Induced Cardioprotection Occurs via Glycogen Synthase Kinase β Inhibition During Reperfusion in Intact Rat Hearts

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• Preconditioning protects by inhibiting the mitochondrial permeability transition.

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• Protein Kinase C&egr; Interacts With and Inhibits the Permeability Transition Pore in Cardiac Mitochondria

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• Role of Cyclic Guanosine Monophosphate in Late Preconditioning in Conscious Rabbits

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• Sildenafil (Viagra) induces powerful cardioprotective effect via opening of mitochondrial K(ATP) channels in rabbits.

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• Zinc Release from Protein Kinase C as the Common Event during Activation by Lipid Second Messenger or Reactive Oxygen*

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• Phosphorylation of Glycogen Synthase Kinase-3&bgr; During Preconditioning Through a Phosphatidylinositol-3-Kinase–Dependent Pathway Is Cardioprotective

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