Oxygen Free Radical Signaling in Ischemic Preconditioninga
- 1 June 1999
- journal article
- Published by Wiley in Annals of the New York Academy of Sciences
- Vol. 874 (1) , 49-65
- https://doi.org/10.1111/j.1749-6632.1999.tb09224.x
Abstract
This review will focus on the free radical signaling mechanism of preconditioning. The results from our laboratory as well as studies from other laboratories suggest that reactive oxygen species function as second messenger during myocardial adaptation to ischemia. This review provides evidence for the first time that tyrosine kinase and MAP kinases are the targets for reactive oxygen species generated in the preconditioned myocardium. The finding that p38 MAP kinase might be upstream of NFκB further supports our previous reports that MAPKAP kinase 2 could be the most likely link between the preconditioning and adaptation mediated by gene expression. p38 activation appears to be an important step in the translocation and activation of the nuclear transcription factor NFκB, which in turn may be involved in the induction of the expression of a variety of stress‐inducible genes.Keywords
This publication has 85 references indexed in Scilit:
- Oxidative stress as a mediator of apoptosisPublished by Elsevier ,2002
- Differential regulation of Bcl‐2, AP‐1 and NF‐κB on cardiomyocyte apoptosis during myocardial ischemic stress adaptationFEBS Letters, 1999
- An essential role of NFκB in tyrosine kinase signaling of p38 MAP kinase regulation of myocardial adaptation to ischemiaFEBS Letters, 1998
- Ischemic preconditioning triggers the activation of MAP kinases and MAPKAP kinase 2 in rat heartsFEBS Letters, 1996
- Transient Overexpression of Catalase Does Not Inhibit TNF- or PMA-Induced NF-κB ActivationBiochemical and Biophysical Research Communications, 1995
- Activation of the MAP kinase homologue RK requires the phosphorylation of Thr‐180 and Tyr‐182 and both residues are phosphorylated in chemically stressed KB cellsFEBS Letters, 1995
- Pretreatment with angiotensin II activates protein kinase C and limits myocardial infarction in isolated rabbit heartsJournal of Molecular and Cellular Cardiology, 1995
- Reperfusion injury induces apoptosis in rabbit cardiomyocytes.Journal of Clinical Investigation, 1994
- A MAP Kinase Targeted by Endotoxin and Hyperosmolarity in Mammalian CellsScience, 1994
- Hypoxic preconditioning attenuates stunning caused by repeated coronary artery occlusions in dog heartCardiovascular Research, 1993