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Oxygen Free Radical Signaling in Ischemic Preconditioning a
Author(s) -
DAS DIPAK K.,
ENGELMAN RICHARD M.,
MAULIK NILANJANA
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb09224.x
Subject(s) - p38 mitogen activated protein kinases , reactive oxygen species , microbiology and biotechnology , transcription factor , kinase , signal transduction , chemistry , ischemic preconditioning , tyrosine kinase , oxygen , ischemia , biology , biochemistry , gene , medicine , protein kinase a , organic chemistry
A bstract : 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.