Metabolic syndrome and mitochondrial dysfunction: insights from preclinical studies with a mitochondrially targeted antioxidant

Abstract

An important emerging area in the translational aspects of redox biology and bioenergetics are the new findings that implicate mitochondrial dysfunction as a key player in the etiology of metabolic syndrome and diabetes. The paper in this issue of Free Radical Biology & Medicine, entitled “The mitochondria-targeted antioxidant MitoQ decreases features of the Metabolic Syndrome in ATM+/−/ApoE−/− mice” by Mercer and colleagues shows, in an elegant pre-clinical study, that mitochondrial therapeutics may be beneficial for this important clinical problem. The work is exciting because it not only validates a role for mitochondrial redox signaling in the etiology of metabolic syndrome but also highlights a potential therapeutic agent to treat metabolic syndrome in human subjects.