The expression of CG9940 affects the adaptation of cardiac function, mobility, and lifespan to exercise in aging Drosophila

Wen, Deng-Tai; Zheng, Lan; Ni, Lei; Wang, Hui; Yue, Feng; Zhang, Min

doi:10.1016/j.exger.2016.07.006

Cited by 22 publications

(29 citation statements)

References 68 publications

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“…Most flies continued to respond by climbing throughout the exercise period. The few that failed to climb were actively walking at the inner wall of the vial [ 17 , 27 ]. Flies were exercised in vials with a 2.8-cm inner diameter, rotated at 0.18 rev/s, 0.20 rev/s, 0.18 rev/s, 0.16 rev/s, and 0.14 rev/s.…”

Section: Methodsmentioning

confidence: 99%

“…A recent study reported that exercise training protects against age-dependent cardiac fibrosis by suppressing AT1R and Nox2 as part of a RAS-Nox2-TGF-beta pathway [ 15 ]. Increasing evidence suggests that exercise training does not only improve health-related-quality of life but also extends the average lifespan [ 16 , 17 ]. These reports indicate that although exercise training has an opposite effect on the body compared with obesity, but there is no direct evidence that lifetime exercise training can totally combat lifetime HFD-induced obesity problems such as locomotor impairment, lipotoxic cardiomyopathy, and decrease in lifespan.…”

Section: Introductionmentioning

confidence: 99%

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Endurance exercise prevents high-fat-diet induced heart and mobility premature aging and dsir2 expression decline in aging Drosophila

et al. 2017

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High-Fat-Diet (HFD)-induced obesity is a major contributor to heart and mobility premature aging and mortality in both Drosophila and humans. The dSir2 genes are closely related to aging, but there are few directed reports showing that whether HFD could inhibit the expression dSir2 genes. Endurance exercise can prevent fat accumulation and reverse HFD-induced cardiac dysfunction. Endurance also delays age-relate functional decline. It is unclear whether lifetime endurance exercise can combat lifetime HFD-induced heart and mobility premature aging, and relieve the harmful HFD-induced influence on the dSir2 gene and lifespan yet. In this study, flies are fed a HFD and trained from when they are 1 week old until they are 5 weeks old. Then, triacylglycerol levels, climbing index, cardiac function, lifespan, and dSir2 mRNA expressions are measured. We show that endurance exercise improves climbing capacity, cardiac contraction, and dSir2 expression, and it reduces body and heart triacylglycerol levels, heart fibrillation, and mortality in both HFD and aging flies. So, lifelong endurance exercise delays HFD-induced accelerated age-related locomotor impairment, cardiac dysfunction, death, and dSir2 expression decline, and prevents HFD-induced premature aging in Drosophila.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Endurance exercise prevents high-fat-diet induced heart and mobility premature aging and dsir2 expression decline in aging Drosophila

et al. 2017

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“…However, we would like to emphasize again that tissue and species discrepancies would have to be more extensively scrutinized to determine potential fundamental differences. Indeed, overexpression of the NAD + synthase CG9940 in flies resulted in a mild but significant extension of lifespan [222]. Consistently, NAD + dependent Sir2 (Sirt1 in mammals) has been implicated in lifespan extension not only in flies but also in yeast and mammals in a tissue-and dose-dependent manner [223][224][225].…”

Section: Crosstalk Between Epigenetics and Metabolism With Agementioning

confidence: 85%

“…A loss in age-related gene silencing of a position effect variegation reporter was also observed upon global mild overexpression of dSir2 [206]. Finally, evidence suggests that replenishing the NAD + pool by overexpressing NAD + synthase decreases arrhythmia and fibrillations in old flies compared to age-matched controls [222]. However, these studies are not entirely conclusive, and the specific roles of NAD + and Sir2 in cardiac aging need to be characterized in greater detail.…”

Section: Crosstalk Between Epigenetics and Metabolism With Agementioning

confidence: 99%

As time flies by: Investigating cardiac aging in the short-lived Drosophila model

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et al. 2019

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…In both mammals and flies, it is well known that aging is accompanied by a decline in locomotion ability (Demontis et al, 2013;Wen et al, 2016). In aging, oxidant production from some sources is increased, antioxidant enzymes are decreased and the adaptive response to oxidative stress is reduced (Liu and Marcinek, 2017).…”

Section: P<0mentioning

confidence: 99%

Endurance exercise protects agingDrosophilafrom high-salt diet(HSD)-induced climbing capacity decline and lifespan decrease by enhancing antioxidant capacity

et al. 2020

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A high-salt diet (HSD) is a major cause of many chronic and agerelated defects such as myocardial hypertrophy, locomotor impairment and mortality. Exercise training can efficiently prevent and treat many chronic and age-related diseases. However, it remains unclear whether endurance exercise can resist HSDinduced impairment of climbing capacity and longevity in aging individuals. In our study, flies were given exercise training and fed a HSD from 1-week old to 5-weeks old. Overexpression or knockdown of salt and dFOXO were built by UAS/Gal4 system. The results showed that a HSD, salt gene overexpression and dFOXO knockdown significantly reduced climbing endurance, climbing index, survival, dFOXO expression and SOD activity level, and increased malondialdehyde level in aging flies. Inversely, in a HSD aging flies, endurance exercise and dFOXO overexpression significantly increased their climbing ability, lifespan and antioxidant capacity, but they did not significantly change the salt gene expression. Overall, current results indicated that a HSD accelerated the age-related decline of climbing capacity and mortality via upregulating salt expression and inhibiting the dFOXO/SOD pathway. Increased dFOXO/SOD pathway activity played a key role in mediating endurance exercise resistance to the low salt tolerance-induced impairment of climbing capacity and longevity in aging Drosophila.

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The expression of CG9940 affects the adaptation of cardiac function, mobility, and lifespan to exercise in aging Drosophila

Cited by 22 publications

References 68 publications

Endurance exercise prevents high-fat-diet induced heart and mobility premature aging and dsir2 expression decline in aging Drosophila

Endurance exercise prevents high-fat-diet induced heart and mobility premature aging and dsir2 expression decline in aging Drosophila

As time flies by: Investigating cardiac aging in the short-lived Drosophila model

Endurance exercise protects agingDrosophilafrom high-salt diet(HSD)-induced climbing capacity decline and lifespan decrease by enhancing antioxidant capacity

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