Review highlights how succinate influences mitochondrial respiratory chain in inflammation, suggesting it aids energy production and acts as a signaling molecule.
This review is devoted to physiological and pathophysiological role of endogenous and exogenous succinate in ensuring effective oxidative phosphorylation process in mitochondrial respiratory chain. The last one ensures synthesis of adenosine triphosphate (ATP) under normoxic and hypoxic conditions. Both endogenous and exogenous succinate performs the same functions in providing substrate for mitochondrial respiratory chain and has no different pharmacological effects. Under hypoxia and inflammation, succinate acts as a signaling molecule indicating severity of hypoxia and inflammation, as well as suppression of oxidative phosphorylation. Accumulation of succinate under hypoxia and inflammation has compensatory and protective (antioxidant) nature that is realized under regression of inflammation through reperfusion and reoxygenation. During these periods, succinate is oxidized faster than synthesized. Exogenous succinate plays a substitute role and functions similar to endogenous substrate providing energy potential of mitochondrial respiratory chain.
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Orlov et al. (2025) studied this question.
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