[SIGNALING MECHANISM OF CARDIOPROTECTIVE EFFECT OF REACTIVE OXYGEN SPECIES].
Protein kinase Cepsilon (PKCepsilon) is a target for reactive oxygen species (ROS). It is activated with reaction products of OH* with phospholipids, which presumably include hydroperoxides of fatty acids or alkylperoxy radicals. Activation of PKCs with reactive oxygen species promotes to mito-K(ATP) channel opening and MPT pore (mitochondrial permeability transition pore) closing thereby it is increasing the resistance of cardiomyocytes to hypoxia-reoxygenation. P38 kinase and tyrosine kinases are targets of ROS. Hydroxyl radical or signaling molecules, resulting from its metabolism, may contribute to the activation of p38-kinase that increases the cardiac tolerance to the impact of ischemia-reperfusion. Src tyrosine kinase and P13-kinase apparently are not targets of ROS. The cardioprotective effect of ROS may be due to the activation of transcription factors NFkappaB and CREB.
L N
LN
Maslov
N V
NV
Naryzhnaya
Yu K
YK
Podoksenov
A S
AS
Sementsov
A S
AS
Gorbunov
D000818:Animals; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D051744:Protein Kinase C-epsilon / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction
D017382:Reactive Oxygen Species; D051744:Protein Kinase C-epsilon