Figure 7.
Schematic of proposed cell death/survival pathway. During ischaemic stress, the UPR kinase PERK is activated, which leads to lysosome-mediated degradation of the SUMO-2/3-specific deSUMOylating enzyme SENP3. The absence of SENP3 prolongs Drp1 SUMOylation, favouring localization in the cytosol and reducing Drp1-mediated cytochrome c release. Following reoxygenation, however, SENP3 levels recover, promoting mitochondrial association of Drp1 and cell death.