Mitochondria hormesis delays aging and associated diseases in Caenorhabditis elegans impacting on key ferroptosis players

The study aimed to investigate the mechanisms that promote compensatory pro-longevity responses during mild mitochondrial stress in Caenorhabditis elegans. This was achieved by performing a DNA microarray analysis to compare gene expression profiles of wild-type and mild mitochondrial-stressed long-lived worms at days 4, 7, and 14 after birth, in five replicates. The worms were fed with either an empty-vector control (pL4440) or vector-expressing dsRNA against nematode frataxin (frh-1) to induce mild mitochondrial stress, for 3 consecutive generation starting from eggs.