The activation of cardiac dSir2-related pathways mediates physical exercise resistance to heart aging in old Drosophila.

摘要: Cardiac aging is majorly characterized by increased diastolic dysfunction, lipid accumulation, oxidative stress, and contractility debility. The Sir2/Sirt1 gene overexpression delays cell reduces obesity stress. Exercise improves heart function aging. However, it remains unclear whether exercise delaying related to cardiac Sir2/Sirt1-related pathways. In this study, dSir2 or knockdown was regulated using the UAS/hand-Gal4 system in Drosophila. Flies underwent interventions from 4 weeks 5 old. Results showed that either remarkably period, systolic interval, fractional shortening, SOD activity, dSIR2 protein, Foxo, dSir2, Nmnat, bmm expression levels flies; they also notably reduced triacylglycerol level, malonaldehyde dysfunction index. Either had almost opposite effects on as those of overexpression. Therefore, we claim delayed promoted reducing increasing age-related activation dSir2/Foxo/SOD dSir2/Foxo/bmm pathways may be two important molecular mechanisms through which works against