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Because rapamycin, which extends mouse lifespan 31 , can reverse age-related diastolic dysfunction and restore a more youthful metabolome in the aged myocardium 32 , we next evaluated metabolomic changes in Young, Old Con, and Old mAb female-treated hearts

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reported that there is a ferroptosis system in mitochondria mainly composed of dihydrolactate dehydrogenase, which also induces lipid peroxidation in the mitochondrial membrane by promoting the reduction of CoQ10 to combat ferroptosis (81)

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