PI3 Kinase and not p42/p44 Appears to be Implicated in the Protection Conferred by Ischemic Preconditioning
- 1 June 2002
- journal article
- Published by Elsevier in Journal of Molecular and Cellular Cardiology
- Vol. 34 (6) , 661-668
- https://doi.org/10.1006/jmcc.2002.2006
Abstract
No abstract availableKeywords
This publication has 33 references indexed in Scilit:
- Insulin Prevents Cardiomyocytes From Oxidative Stress–Induced Apoptosis Through Activation of PI3 Kinase/ AktCirculation, 2000
- Caspase inhibition and limitation of myocardial infarct size: protection against lethal reperfusion injuryBritish Journal of Pharmacology, 2000
- Apoptosis is Initiated by Myocardial Ischemia and Executed During ReperfusionJournal of Molecular and Cellular Cardiology, 2000
- Reperfusion Injury Revisited Is There a Role for Growth Factor Signaling in Limiting Lethal Reperfusion Injury?Trends in Cardiovascular Medicine, 1999
- Caspase Inhibition Reduces Myocyte Cell Death Induced by Myocardial Ischemia and Reperfusion In VivoJournal of Molecular and Cellular Cardiology, 1999
- Phosphatidylinositol 3-Kinase Regulates Differentiation of H9c2 Cardiomyoblasts Mainly through the Protein Kinase B/Akt-Independent PathwayArchives of Biochemistry and Biophysics, 1999
- Regulation of Cell Death Protease Caspase-9 by PhosphorylationScience, 1998
- Ischemic preconditioning attenuates apoptotic cell death associated with ischemia/reperfusionMolecular and Cellular Biochemistry, 1998
- Ischemic preconditioning slows energy metabolism and delays ultrastructural damage during a sustained ischemic episode.Circulation Research, 1990
- Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.Circulation, 1986