[Intracellular mechanisms of cardioprotection during adaptation to hypoxia. Triggers and kinase cascades].

N. V. Naryzhnaǐa, Y. B. Lishmanov, F. Kolar, L. N. Maslov, I. Zhang, A. G. Portnichenko

Research output: Contribution to journalArticlepeer-review


Adaptation to chronic hypoxia increases myocardial ischemic tolerance to injury caused by acute ischemia-reperfusion. In this article, we provide a brief overview of current literary data dealing with signalling mechanisms that can play a certain role in chronic hypoxia-induced cardioprotection. It has been shown that reactive oxygen species are major contributors to induction of the protective cardiac phenotype. In this context, we discuss the role of cytochromes, NADPH oxidase, heme oxygenase-1, mitochondrial monoamme oxidase, and prolyl 4-hydroxylase in triggering adaptive responses resulting in myocardial salvage. Moreover, we point to other cytoprotective proteins that can be involved in the protection from chronic hypoxia, such as protein kinase C, mitogen-activated protein kinases, 5'AMP-activated protein kinase, NO-synthases, mitochondrial ATP-sensitive K+ channels, Ca(2+)-activated large-conductance K+ channels, and MPT pore. Understanding the molecular mechanism of this long-lasting form of cardioprotection may help in providing basis for development of future therapeutic strategies to protect ischemic heart.

Original languageEnglish
Pages (from-to)923-938
Number of pages16
JournalRossiǐskii fiziologicheskiǐ zhurnal imeni I.M. Sechenova / Rossiǐskaia akademiia nauk
Issue number9
Publication statusPublished - Sep 2011

ASJC Scopus subject areas

  • Physiology

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