Mitochondria in the Aging Muscles of Flies and Mice: New Perspectives for Old Characters

Campo, Andrea del; Jaimovich, Enrique; Tevy, María Florencia

doi:10.1155/2016/9057593

Cited by 15 publications

(16 citation statements)

References 107 publications

(115 reference statements)

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“…The other widely used phenotypic marker of aging is the age-related decline of motility. Decreased motility with aging is associated with muscle atrophy and dysfunction [40]. Recent studies have shown that genetic intervention with antioxidant genes, such as cat and sod-1 , or nutritional intervention with antioxidants, such as silymarin and selenocysteine, can modulate age-related muscle dysfunction [16, 41, 42].…”

Section: Discussionmentioning

confidence: 99%

Phosphatidylcholine Extends Lifespan via DAF-16 and Reduces Amyloid-Beta-Induced Toxicity inCaenorhabditis elegans

Kim

Park

2019

Oxidative Medicine and Cellular Longevity

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Phosphatidylcholine is one of the major phospholipids comprising cellular membrane and is known to have several health-promoting activities, including the improvement of brain function and liver repair. In this paper, we examine the in vivo effect of dietary supplementation with phosphatidylcholine on the response to environmental stressors and aging in C. elegans. Treatment with phosphatidylcholine significantly increased the survival of worms under oxidative stress conditions. However, there was no significant difference in response to stresses caused by heat shock or ultraviolet irradiation. Oxidative stress is believed to be one of the major causal factors of aging. Then, we examined the effect of phosphatidylcholine on lifespan and age-related physiological changes. Phosphatidylcholine showed a lifespan-extending effect and a reduction in fertility, possibly as a tradeoff for long lifespan. Age-related decline of motility was also significantly delayed by supplementation with phosphatidylcholine. Interestingly, the expressions of well-known longevity-assuring genes, hsp-16.2 and sod-3, were significantly upregulated by dietary intervention with phosphatidylcholine. DAF-16, a transcription factor modulating stress response genes, was accumulated in the nucleus by phosphatidylcholine treatment. Increase of the ROS level with phosphatidylcholine suggests that the antioxidant and lifespan-extending effects are due to the hormetic effect of phosphatidylcholine. Phosphatidylcholine also showed a protective effect against amyloid beta-induced toxicity in Alzheimer’s disease model animals. Experiments with long-lived mutants revealed that the lifespan-extending effect of phosphatidylcholine specifically overlapped with that of reduced insulin/IGF-1-like signaling and required DAF-16. These findings showed the antioxidant and antiaging activities of phosphatidylcholine for the first time in vivo. Further studies focusing on the identification of underlying cellular mechanisms involved in the antiaging effect will increase the possibility of using phosphatidylcholine for the development of antiaging therapeutics.

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Section: Discussionmentioning

confidence: 99%

Phosphatidylcholine Extends Lifespan via DAF-16 and Reduces Amyloid-Beta-Induced Toxicity inCaenorhabditis elegans

Kim

Park

2019

Oxidative Medicine and Cellular Longevity

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“…There are many reasons for the increase in ROS; the decreased cellular antioxidant capacity caused by decreased antioxidant enzyme (superoxide dismutase, catalase and glutathione peroxidase) activity [15] is an important factor leading to increased ROS production. Studies have shown that the activity of antioxidant enzymes is gradually reduced during the process of skeletal muscle aging [15]. The overexpression of skeletal muscle catalase in aged mice can improve age-related mitochondrial oxidative stress and dysfunction, and enhance mitochondrial energy metabolism [4].…”

Section: Oxidative Stress Levels Increase In Aging Skeletal Musclementioning

confidence: 99%

Mechanism of increased risk of insulin resistance in aging skeletal muscle

Shou

Chen

Xiao

2020

Diabetol Metab Syndr

146

112

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As age increases, the risk of developing type 2 diabetes increases, which is associated with senile skeletal muscle dysfunction. During skeletal muscle aging, mitochondrial dysfunction, intramyocellular lipid accumulation, increased inflammation, oxidative stress, modified activity of insulin sensitivity regulatory enzymes, endoplasmic reticulum stress, decreased autophagy, sarcopenia and over-activated renin-angiotensin system may occur. These changes can impair skeletal muscle insulin sensitivity and increase the risk of insulin resistance and type 2 diabetes during skeletal muscle aging. This review of the mechanism of the increased risk of insulin resistance during skeletal muscle aging will provide a more comprehensive explanation for the increased incidence of type 2 diabetes in elderly individuals, and will also provide a more comprehensive perspective for the prevention and treatment of type 2 diabetes in elderly populations.

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“…Disturbances in calcium regulation and mitochondrial homeostasis may also contribute to the decline of muscle performance in aging (for review, see Del Campo, Jaimovich, & Tevy, 2016). Indeed, Pietrangelo et al.…”

Section: Regulating Factors Of Mptp and Agingmentioning

confidence: 99%

Mitochondria and aging: A role for the mitochondrial transition pore?

2018

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SummaryThe cellular mechanisms responsible for aging are poorly understood. Aging is considered as a degenerative process induced by the accumulation of cellular lesions leading progressively to organ dysfunction and death. The free radical theory of aging has long been considered the most relevant to explain the mechanisms of aging. As the mitochondrion is an important source of reactive oxygen species (ROS), this organelle is regarded as a key intracellular player in this process and a large amount of data supports the role of mitochondrial ROS production during aging. Thus, mitochondrial ROS, oxidative damage, aging, and aging‐dependent diseases are strongly connected. However, other features of mitochondrial physiology and dysfunction have been recently implicated in the development of the aging process. Here, we examine the potential role of the mitochondrial permeability transition pore (mPTP) in normal aging and in aging‐associated diseases.

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Mitochondria in the Aging Muscles of Flies and Mice: New Perspectives for Old Characters

Cited by 15 publications

References 107 publications

Phosphatidylcholine Extends Lifespan via DAF-16 and Reduces Amyloid-Beta-Induced Toxicity inCaenorhabditis elegans

Phosphatidylcholine Extends Lifespan via DAF-16 and Reduces Amyloid-Beta-Induced Toxicity inCaenorhabditis elegans

Mechanism of increased risk of insulin resistance in aging skeletal muscle

Mitochondria and aging: A role for the mitochondrial transition pore?

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