Because of the extent of succinate accumulation during ischemia, succinate is exchanged from mitochondria into the cytosol, where it can act to inhibit prolyl hydroxylases (PHD) involved in the degradation of hypoxia-inducible factor 1α (HIF-1α). As HIF escapes degradation, it can translocate to the nucleus and promote the transcription of a number of genes involved in the hypoxic response. Inhibiting SDH with dimethyl malonate prevents the accumulation of succinate during ischemia.