Oxygen Free Radical Signaling in Ischemic Preconditioninga

Authors

  • DIPAK K. DAS,

    1. University of Connecticut School of Medicine, Farmington, Connecticut, USA Baystate Medical Center, Springfield, Massachusetts, USA
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  • RICHARD M. ENGELMAN,

    1. University of Connecticut School of Medicine, Farmington, Connecticut, USA Baystate Medical Center, Springfield, Massachusetts, USA
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  • NILANJANA MAULIK

    1. University of Connecticut School of Medicine, Farmington, Connecticut, USA Baystate Medical Center, Springfield, Massachusetts, USA
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  • a

    This study was supported by National Institutes of Health grants HL 34360, HL 22559, HL 33889, HL 56803, as well as by a Grant-in-Aid from the American Heart Association.

Abstract

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.

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