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International Journal of Physiology and Pathophysiology
SJR: 0.106

ISSN Imprimer: 2155-014X
ISSN En ligne: 2155-0158

Archives: Volume 1, 2010 to Volume 9, 2018

International Journal of Physiology and Pathophysiology

DOI: 10.1615/IntJPhysPathophys.v5.i4.90
pages 363-381

Mitochondria Signaling in Adaptation to Hypoxia

Ludmila D. Lukyanova
Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow, Russia

RÉSUMÉ

A bioenergetic mechanism for development of urgent adaptation to hypoxia is considered. Hypoxia induces reprogramming of respiratory chain function and switching from oxidation of NAD-related substrates (complex I) to succinate oxidation (complex II). Transient, reversible, compensatory activation of respiratory chain complex II is a major mechanism of urgent adaptation to hypoxia necessary for 1) succinate-related energy synthesis in conditions of oxygen deficiency and formation of urgent resistance in the body; 2) succinate-related stabilization of HIF-1 α and initiation of its transcriptional activity related with formation of urgent and long-term adaptation; 3) succinate-related activation of a succinate-specific receptor GPR91. Therefore, succinate is a signaling molecule, and its effects are realized at three levels in hypoxia, intramitochondrial, intracellular and intercellular.


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