« Previous
Next »
Trends in Cardiovascular Medicine
Volume 15, Issue 2
, Pages 69-75
, February 2005
The Reperfusion Injury Salvage Kinase Pathway: A Common Target for Both Ischemic Preconditioning and Postconditioning
References
- . Postconditioning inhibits mitochondrial permeability transition. Circulation. 2005;18:194–197
- Protein kinase C-ɛ interacts with and inhibits the permeability transition pore in cardiac mitochondria. Circ Res. 2003;92:873–880
- Mitochondrial PKCɛ and MAPK form signaling modules in the murine heart: Enhanced mitochondrial PKCɛ-MAPK interactions and differential MAPK activation in PKCɛ-induced cardioprotection. Circ Res. 2002;90:390–397
- Inconsistent relation of MAPK activation to infarct size reduction by ischemic preconditioning in pigs. Am J Physiol. 2000;279:H1111–H1119
- . Atorvastatin, administered at the onset of reperfusion, and independent of lipid lowering, protects the myocardium by up-regulating a pro-survival pathway. J Am Coll Cardiol. 2003;41:508–515
- . Bradykinin limits infarction when administered as an adjunct to reperfusion in mouse heart: the role of PI3K, Akt and eNOS. J Mol Cell Cardiol. 2003;35:185–193
- . Myocardial reperfusion: a double-edged sword?. J Clin Invest. 1985;76:1713–1719
- Concentration-dependent effects of nitric oxide on mitochondrial permeability transition and cytochrome c release. J Biol Chem. 2000;275:20474–20479
- Insulin inhibits opening of the mitochondrial permeability transition pore via the reperfusion injury salvage kinase (RISK) pathway. Circulation. 2004;100:131
- . Glucose-insulin-potassium therapy for treatment of acute myocardial infarction: an overview or randomized placebo-controlled trials. Circulation. 1997;96:1152–1156
- Apoptosis is initiated by myocardial ischemia and executed during reperfusion. J Mol Cell Cardiol. 2000;32:197–208
- Differential activation of extracellular signal regulated kinase isoforms in preconditioning and opioid-induced cardioprotection. J Pharmacol Exp Ther. 2001;296:642–649
- . Akt promotes survival of cardiomyocytes against ischemia–reperfusion injury in mouse heart. Circulation. 2000;101:660–667
- Reperfusion injury induces apoptosis in rabbit cardiomyocytes. J Clin Invest. 1994;94:1621–1628
- . Opioid-induced cardioprotection occurs via glycogen synthase kinase beta inhibition during reperfusion in intact rat hearts. Circ Res. 2004;94:960–966
- Inhibiting mitochondrial permeability transition pore opening: a new paradigm for myocardial preconditioning?. Cardiovasc Res. 2002;55:534–543
- . The mitochondrial permeability transition pore: its fundamental role in mediating cell death during ischaemia and reperfusion. J Mol Cell Cardiol. 2003;35:339–341
- . New directions for protecting the heart against ischaemia–reperfusion injury: targeting the Reperfusion Injury Salvage Kinase (RISK)-pathway. Cardiovasc Res. 2004;61:448–460
- Preconditioning protects by inhibiting the mitochondrial permeability transition. Am J Physiol. 2004;287:H841–H849
- Ischemic preconditioning protects by activating pro-survival kinases at reperfusion. Am J Physiol. 2005;288:H971–H976
- . Postconditioning: old wine in a new bottle?. J Am Coll Cardiol. 2004;44:1111–1112
- Myocardial protection by insulin at reperfusion requires early administration and is mediated via Akt and p70s6 kinase cell-survival signaling. Circ Res. 2001;89:1191–1198
- Glycogen synthase kinase-3β mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore. J Clin Invest. 2004;113:1535–1549
- Cardioprotection by “postconditioning” is mediated by increased retention of endogenous intravascular adenosine and activation of A2A receptors during reperfusion. Circulation. 2004;100:803
- Postconditioning attenuates myocardial ischemia–reperfusion injury by inhibiting events in the early minutes of reperfusion. Cardiovasc Res. 2004;62:74–85
- ACh and adenosine activate PI3-kinase in rabbit hearts through transactivation of receptor tyrosine kinases. Am J Physiol. 2002;283:H2322–H2330
- Mitochondrial ROS generation following acetylcholine-induced EGF receptor transactivation requires metalloproteinase cleavage of proHB-EGF. J Mol Cell Cardiol. 2004;36:435–443
- Acetylcholine and bradykinin trigger preconditioning in the heart through a pathway that includes Akt and NOS. Am J Physiol. 2004;287:H2606–H2611
- Effect of glucose-insulin-potassium infusion on mortality in patients with acute ST-segment elevation myocardial infarction: The CREATE-ECLA randomized controlled trial. JAMA. 2005;293:437–446
- Intracoronary adenovirus-mediated Akt gene transfer in hearts limits infarct size following ischemia–reperfusion injury. J Mol Cell Cardiol. 2000;32:2397–2402
- . PI3 kinase and not p42/p44 appears to be implicated in the protection conferred by ischemic preconditioning. J Mol Cell Cardiol. 2002;34:661–668
- . Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation. 1986;74:1124–1136
- Effects of glucagon-like peptide-1 in patients with acute myocardial infarction and left ventricular dysfunction after successful reperfusion. Circulation. 2004;109:962–965
- Reperfusion conditions: importance of ensuring gentle versus sudden reperfusion during relief of coronary occlusion. J Thorac Cardiovasc Surg. 1986;92:613–620
- Bradykinin induces mitochondrial ROS generation via NO, cGMP, PKG, and mitoKATP channel opening and leads to cardioprotection. Am J Physiol. 2004;286:H468–H476
- . Postconditioning must be initiated in less than 1 minute following reperfusion and is dependent on adenosine receptors and PI3-kinase. Circulation. 2004;100:804
- Mitochondrial K(ATP) channel openers activate the ERK kinase by an oxidant-dependent mechanism. Am J Physiol. 2002;283:C273–C281
- . Urocortin protects the heart from reperfusion injury via upregulation of p42/p44 MAPK signaling pathway. Am J Physiol. 2002;283:H1481–H1488
- . PI3 kinase supports the preconditioned heart through a critical convalescent period. JMCC. 2005;(submitted)
- Ischemic preconditioning activates phosphatidylinositol-3-kinase upstream of protein kinase C. Circ Res. 2000;87:309–315
- Phosphorylation of glycogen synthase kinase-3beta during preconditioning through a phosphatidylinositol-3-kinase-dependent pathway is cardioprotective. Circ Res. 2002;90:377–379
- Postconditioning: a form of “modified reperfusion” protects the myocardium by activating the phosphatidylinositol 3-kinase-Akt pathway. Circ Res. 2004;95:230–232
- . The phosphatidylinositol 3-kinase (PI3K)-Akt pathway suppresses Bax translocation to mitochondria. J Biol Chem. 2002;277:14040–14047
- NECA and bradykinin at reperfusion reduce infarction in rabbit hearts by signaling through PI3K, ERK, and NO. J Mol Cell Cardiol. 2004;36:411–421
- Multiple, brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways. J Am Coll Cardiol. 2004;44:1103–1110
- . Reperfusion injury revisited: is there a role for growth factor signaling in limiting lethal reperfusion injury?. Trends Cardiovasc Med. 1999;9:245–249
- Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol. 2003;285:H579–H588
PII: S1050-1738(05)00025-3
doi: 10.1016/j.tcm.2005.03.001
© 2005 Elsevier Inc. All rights reserved.
« Previous
Next »
Trends in Cardiovascular Medicine
Volume 15, Issue 2
, Pages 69-75
, February 2005
