Oxygen free radical signaling in ischemic preconditioning.
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 NF kappa B 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 NF kappa B, which in turn may be involved in the induction of the expression of a variety of stress-inducible genes.
University of Connecticut School of Medicine, Farmington, USA.
D K
DK
Das
R M
RM
Engelman
N
N
Maulik
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D015870:Gene Expression / Q000502:physiology; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D011493:Protein Kinase C / Q000502:physiology; D017382:Reactive Oxygen Species / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*
D017382:Reactive Oxygen Species; D011493:Protein Kinase C