[Signaling mechanism of NO-induced increase in cardiac tolerance to ischemia-reperfusion].
In the review it is analyzes published data on the signaling mechanism of cardioprotective impact of nitric oxide. It was shown that nitric oxide exhibited a rapid and a delayed cardioprotective effects. In the rapid effect, endothelial NO-synthase (NOS) is involved was involved as well as guanylate cyclase, cGMP, kinase G, kinase C, PI3-kinase, Akt-kinase, mitochondrial ATP-sensitive K+-channel, reactive oxygen species, MPT-pore. Delayed cardioprotective effect of NOS required synthesis of proteins de novo. In this process, transcription factors NF-KB, STAT1/3, HIF-1 are involved. Some published data state that peroxynitrite, cGMP, kinase G, kinase C, Src kinase, p38 kinase, ERK-kinase can be involved in delayed cardioprotective effect of NOS. The cardioprotective impact of nitric oxide was shown to depend on enhancement in expression of NOS, cyclooxygenase-2 and Blc-2 protein which inhibits MPT-pore.
Maslov
L N
LN
Kolar
F
F
Barzakh
E I
EI
D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D011494:Protein Kinases / Q000378:metabolism*; D015427:Reperfusion Injury / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology; D014157:Transcription Factors / Q000378:metabolism*
D020030:Nitric Oxide Donors; D014157:Transcription Factors; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D011494:Protein Kinases