title: [Mithochondria signaling in adaptation to hypoxia].
abstract: 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-1alpha 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.
authors.forename: L D
authors.initials: LD
authors.lastname: Luk'ianova
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D042967:Electron Transport Complex I / Q000378:metabolism; D042963:Electron Transport Complex II / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism / Q000502:physiology*; D010101:Oxygen Consumption / Q000502:physiology; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D043562:Receptors, G-Protein-Coupled; D042963:Electron Transport Complex II; D042967:Electron Transport Complex I