Mitochondria-targeted drugs enhance Nlrp3 inflammasome-dependent IL-1β secretion in association with alterations in cellular redox and energy status

► Nlrp3 inflammasome activation caused by SAA involves mitochondrial reactive oxygen species. ► A mechanism by which mitochondrial dysfunction causes sustained IL-1β is proposed. ► The mechanism is based on impaired Nlrp3 complex disassembly.