Myocardial protection against reperfusion injury: The cGMP pathway

No abstract is available for this paper.

• Publication year

  2009

• Venue

  Thrombosis and Haemostasis

• Publication date

  2009-03-13

• Fields of study

  Medicine

• Identifiers
  DOI 10.1160/TH08-11-0764PMID 19350105
• 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.

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• Opening of mitochondrial permeability transition pore induces hypercontracture in Ca2+ overloaded cardiac myocytes

  2007cited by this paper
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• The role of oxidants and free radicals in reperfusion injury.

  2006cited by this paper
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  2006cited by this paper
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  2006cited by this paper
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  2006cited by this paper
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  2006cited by this paper
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  2005cited by this paper
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  2005cited by this paper
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  2005cited by this paper
• Mechanism of cGMP-mediated protection in a cellular model of myocardial reperfusion injury.

  2005cited by this paper
• Calpain-Mediated Impairment of Na+/K+–ATPase Activity During Early Reperfusion Contributes to Cell Death After Myocardial Ischemia

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• Protein Kinase G Transmits the Cardioprotective Signal From Cytosol to Mitochondria

  2005cited by this paper
• Ischemic preconditioning protects by activating prosurvival kinases at reperfusion.

  2005cited by this paper
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• Modulation of soluble guanylate cyclase activity by phosphorylation.

  2004cited by this paper
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• Bradykinin induces mitochondrial ROS generation via NO, cGMP, PKG, and mitoKATP channel opening and leads to cardioprotection.

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

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  2003cited by this paper
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  2003cited by this paper
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  2003cited by this paper
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• Hypoxia and acidosis impair cGMP synthesis in microvascular coronary endothelial cells.

  2002cited by this paper
• ACh and adenosine activate PI3-kinase in rabbit hearts through transactivation of receptor tyrosine kinases.

  2002cited by this paper
• Calcium-dependent membrane association sensitizes soluble guanylyl cyclase to nitric oxide

  2002cited by this paper
• Effect of inhibition of Na(+)/Ca(2+) exchanger at the time of myocardial reperfusion on hypercontracture and cell death.

  2002cited by this paper
• Molecular determinants of the interaction between the inositol 1,4,5-trisphosphate receptor-associated cGMP kinase substrate (IRAG) and cGMP kinase Ibeta.

  2001cited by this paper
• Sub-second Kinetics of the Nitric Oxide Receptor, Soluble Guanylyl Cyclase, in Intact Cerebellar Cells*

  2001cited by this paper
• Intravenous administration of the natriuretic peptide urodilatin at low doses during coronary reperfusion limits infarct size in anesthetized pigs.

  2001cited by this paper
• Role of the reverse mode of the Na+/Ca2+ exchanger in reoxygenation-induced cardiomyocyte injury.

  2001cited by this paper
• Opening of the Mitochondrial Permeability Transition Pore Causes Depletion of Mitochondrial and Cytosolic NAD+and Is a Causative Event in the Death of Myocytes in Postischemic Reperfusion of the Heart*

  2001cited by this paper
• Molecular Determinants of the Interaction between the Inositol 1,4,5-Trisphosphate Receptor-associated cGMP Kinase Substrate (IRAG) and cGMP Kinase Iβ* 210

  2001cited by this paper
• Intravenous atrial natriuretic peptide prevents left ventricular remodeling in patients with first anterior acute myocardial infarction.

  2001cited by this paper
• Urodilatin limits acute reperfusion injury in the isolated rat heart.

  2000cited by this paper
• Dynamic intracoronary thrombosis does not cause significant downstream platelet embolization.

  2000cited by this paper
• Guanylyl cyclases and signaling by cyclic GMP.

  2000cited by this paper
• L-Arginine administration prevents reperfusion-induced cardiomyocyte hypercontracture and reduces infarct size in the pig.

  2000cited by this paper
• Amelioration by quinapril of myocardial infarction induced by coronary occlusion/reperfusion in a rabbit model of atherosclerosis: possible mechanisms.

  1999cited by this paper
• L-arginine inhibits ischemia-reperfusion lung injury in rabbits.

  1999cited by this paper
• Propagation of cardiomyocyte hypercontracture by passage of Na(+) through gap junctions.

  1999cited by this paper
• l-Arginine limits myocardial cell death secondary to hypoxia-reoxygenation by a cGMP-dependent mechanism.

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  1995cited by this paper
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