Abstract
Hypoxia is a typical pathological process characterized by the occurrence of oxygen deficiency in tissues and cells and accompanied by the development of immediate and delayed compensatory and adaptive reactions. Reprogramming of the mitochondrial electron transport chain (ETC) function is one the most essential regulatory mechanisms that allow for immediate adaptation to hypoxia. Succinic acid, or succinate, is involved in this process not only as one of the intermediates of the tricarboxylic acid (TAC) cycle, but also as a signaling molecule. In this connection, the purpose of this review was to systematize the available data on the molecular mechanisms for the development of hypoxia and its adaptation at the ETC/TAC coupling site, as well as on the role of succinic acid in these processes.
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