Mitochondrial Metabolism in Aging Heart.

摘要: Altered mitochondrial metabolism is the underlying basis for increased sensitivity in aged heart to stress. The exhibits impaired metabolic flexibility, with a decreased capacity oxidize fatty acids and enhanced dependence on glucose metabolism. Aging impairs oxidative phosphorylation, greater role played by mitochondria located between myofibrils, interfibrillar mitochondria. With aging, there decrease activity of complexes III IV, which account respiration. Furthermore, aging decreases content among myofibrils. end result that area, ≈50% function, affecting all substrates. defective persist heart, leading oxidant production injury activation signaling cell death. defects represent new therapeutic targets, whether manipulation proteome, modulation electron transport, biogenesis or mitophagy, regulation fission fusion. These mechanisms provide ways attenuate cardiac disease elders preemptive treatment age-related defects, contrast disease-induced dysfunction.