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首页> 外文期刊>Biology Open >Endurance exercise resistance to lipotoxic cardiomyopathy is associated with cardiac NAD+/dSIR2/PGC-1α pathway activation in old Drosophila
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Endurance exercise resistance to lipotoxic cardiomyopathy is associated with cardiac NAD+/dSIR2/PGC-1α pathway activation in old Drosophila

机译：耐运动性对脂毒性心肌病的抵抗力与老年果蝇中的心脏NAD + / dSIR2 /PGC-1α途径活化有关

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摘要

Lipotoxic cardiomyopathy is caused by excessive lipid accumulation in myocardial cells and it is a form of cardiac dysfunction. CardiacPGC-1αoverexpression prevents lipotoxic cardiomyopathy induced by a high-fat diet (HFD). The level of NAD+andSir2expression upregulate the transcriptional activity of PGC-1α. Exercise improves cardiac NAD+level and PGC-1α activity. However, the relationship between exercise, NAD+/dSIR2/PGC-1αpathway and lipotoxic cardiomyopathy remains unknown. In this study, flies were fed a HFD and exercised. The heartdSir2gene was specifically expressed or knocked down by UAS/hand-Gal4 system. The results showed that either a HFD ordSir2knockdown remarkably increased cardiac TG level anddFASexpression, reduced heart fractional shortening and diastolic diameter, increased arrhythmia index, and decreased heart NAD+level, dSIR2 protein,dSir2andPGC-1αexpression levels. Contrarily, either exercise ordSir2overexpression remarkably reduced heart TG level,dFASexpression and arrhythmia index, and notably increased heart fractional shortening, diastolic diameter, NAD+level, dSIR2 level, and heartdSir2andPGC-1αexpression. Therefore, we declared that exercise training could improve lipotoxic cardiomyopathy induced by a HFD or cardiacdSir2knockdown in oldDrosophila. The NAD+/dSIR2/PGC-1αpathway activation was an important molecular mechanism of exercise resistance against lipotoxic cardiomyopathy.
机译：脂毒性心肌病是由心肌细胞中过多的脂质蓄积引起的，是心脏功能障碍的一种形式。 CardiacPGC-1α的过度表达可防止高脂饮食（HFD）引起的脂毒性心肌病。 NAD +和Sir2表达水平上调PGC-1α的转录活性。运动可改善心脏NAD +水平和PGC-1α活性。然而，运动，NAD + / dSIR2 /PGC-1α途径与脂毒性心肌病之间的关系仍然未知。在这项研究中，为果蝇喂食了HFD并进行了锻炼。通过UAS / hand-Gal4系统特异性表达或敲除heartdSir2基因。结果表明，HFD ordSir2基因敲低显着增加了心脏TG水平和dFAS表达，降低了心脏分数缩短和舒张直径，增加了心律失常指数，并降低了心脏NAD +水平，dSIR2蛋白，dSir2和PGC-1α表达水平。相反，运动ordSir2过表达会显着降低心脏TG水平，dFAS表达和心律失常指数，并显着增加心脏分数缩短，舒张直径，NAD +水平，dSIR2水平以及heartdSir2和PGC-1α的表达。因此，我们宣布运动训练可以改善由果蝇中的HFD或heartdSir2基因敲低引起的脂毒性心肌病。 NAD + / dSIR2 /PGC-1α信号通路的激活是运动抵抗脂毒性心肌病的重要分子机制。

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