Short-Term Calorie Restriction Enhances Skeletal Muscle Stem Cell Function

Cerletti, Massimiliano; Jang, Young C.; Finley, Lydia W.S.; Haigis, Marcia C.; Wagers, Amy J.

doi:10.1016/j.stem.2012.04.002

Cited by 336 publications

(316 citation statements)

References 33 publications

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“…30 Multiple lines of evidence indicate that autophagy diminishes with aging, 31 premature aging correlates with autophagy inhibition, 29 while increased autophagy (as by mean of calorie restriction) delays aging and extends longevity. 32,33 Of note, the evidence that calorie restriction enhances MuSCs availability and activity 34 indicates a close relationship between autophagy, the regenerative potential of skeletal muscles, MuSCs activation 35 and self-renewal. 36 A progressive reduction of basal autophagy from young to old and geriatric MuSCs triggering numerical and functional MuSCs decline during ageing has been recently described.…”

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confidence: 99%

Autophagy regulates satellite cell ability to regenerate normal and dystrophic muscles

et al. 2016

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Autophagy is emerging as a key regulatory process during skeletal muscle development, regeneration and homeostasis, and deregulated autophagy has been implicated in muscular disorders and age-related muscle decline. We have monitored autophagy in muscles of mdx mice and human Duchenne muscular dystrophy (DMD) patients at different stages of disease. Our data show that autophagy is activated during the early, compensatory regenerative stages of DMD. A progressive reduction was observed during mdx disease progression, in coincidence with the functional exhaustion of satellite cell-mediated regeneration and accumulation of fibrosis. Moreover, pharmacological manipulation of autophagy can influence disease progression in mdx mice. Of note, studies performed in regenerating muscles of wild-type mice revealed an essential role of autophagy in the activation of satellite cells upon muscle injury. These results support the notion that regeneration-associated autophagy contributes to the early compensatory stage of DMD progression, and interventions that extend activation of autophagy might be beneficial in the treatment of DMD. Thus, autophagy could be a 'disease modifier' targeted by interventions aimed to promote regeneration and delay disease progression in DMD.

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confidence: 99%

Autophagy regulates satellite cell ability to regenerate normal and dystrophic muscles

et al. 2016

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“…Similarly, it has been shown that myogenin expression is not affected after fasting in juvenile gilthead sea bream (Garcia de la Serrana et al, 2014). In line with the lasting production of myofibres in atrophied muscle, it is interesting to note that the catabolic response induced by shortterm calorie restriction is favourable to myogenic cell activation and muscle repair in mouse (Cerletti et al, 2012). Furthermore, the induction of autophagy in muscle satellite cells is crucial to meet bioenergetic demands during the transition from quiescence to activation (Tang and Rando, 2014).…”

Section: Discussionmentioning

confidence: 86%

Analysis of muscle fibre input dynamics using amyog: GFP transgenic trout model

Rescan

Rallière

Lebret

et al. 2015

Journal of Experimental Biology

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The dramatic increase in myotomal muscle mass in teleosts appears to be related to their sustained ability to produce new fibres in the growing myotomal muscle. To describe muscle fibre input dynamics in trout (Oncorhynchus mykiss), we generated a stable transgenic line carrying green fluorescent protein (GFP) cDNA driven by the myogenin promoter. In this myog:GFP transgenic line, muscle cell recruitment is revealed by the appearance of fluorescent, small, nascent muscle fibres. The myog:GFP transgenic line displayed fibre formation patterns in the developing trout and showed that the production of new fluorescent myofibres (muscle hyperplasia) is prevalent in the juvenile stage but progressively decreases to eventually cease at approximately 18 months post-fertilisation. However, fluorescent, nascent myofibres were formed de novo in injured muscle of aged trout, indicating that the inhibition of myofibre formation associated with trout ageing cannot be attributed to the lack of recruitable myogenic cells but rather to changes in the myogenic cell microenvironment. Additionally, the myog:GFP transgenic line demonstrated that myofibre production persists during starvation.

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“…(182) Altogether, these indings provide evidence for the feasibility of targeting SIRT1 as an effective therapeutic intervention for the prevention or reversal of age-related sarcopenia and other degenerative muscle disorders. Encouraging results regarding the use of short-term calorie restriction, a dietary manipulation that increases SIRT1 activity (183), and synthetic small-molecule activators of SIRT1 (184) show muscle stem cell differentiation and improved muscle quality in laboratory animals.…”

Section: Rejuvenating Aged Muscle Stem Cellsmentioning

confidence: 99%

Molecular Regulation and Rejuvenation of Muscle Stem (Satellite) Cell Aging

2015

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BACKGROUND: Age-related muscle loss leads to lack of muscle strength, resulting in reduced posture and mobility and an increased risk of falls, all of which contribute to a decrease in quality of life. Skeletal muscle regeneration is a complex process, which is not yet completely understood.CONTENT: Skeletal muscle undergoes a progressive agerelated loss in mass and function. Preservation of muscle mass depends in part on satellite cells, the resident stem cells of skeletal muscle. Reduced satellite cell function may contribute to the age-associated decrease in muscle mass. Recent studies have delineated that the aging process in organ stem cells is largely caused by age-speciic changes in the differentiated niches, and that regenerative outcomes often depend on the age of the niche, rather than on stem cell age. It is likely that epigenetic states will be better deine such key satellite cell features as prolonged quiescence and lineage idelity. It is also likely that DNA and histone modiications will underlie many of the changes in aged satellite cells that account for age-related declines in functionality and rejuvenation through exposure to the systemic environment. SUMMARY:Skeletal muscle aging results in a gradual loss of skeletal muscle mass, skeletal muscle function and regenerative capacity, which can lead to sarcopenia and increased mortality. Although the mechanisms underlying sarcopenia remain unclear, the skeletal muscle stem cell, or satellite cell, is required for muscle regeneration. Decreased muscle stem cell function in aging has long been shown to depend on altered environmental cues, whereas the contribution of intrinsic mechanisms remained less clear. Signals in the aged niche were shown to cause permanent defects in the ability of satellite cells to return to quiescence, ultimately also impairing the maintenance of self-renewing satellite cells. Therefore, only anti-aging strategies taking both factors, the stem cell niche and the stem cells per se, into consideration may ultimately be successful.

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Short-Term Calorie Restriction Enhances Skeletal Muscle Stem Cell Function

Cited by 336 publications

References 33 publications

Autophagy regulates satellite cell ability to regenerate normal and dystrophic muscles

Autophagy regulates satellite cell ability to regenerate normal and dystrophic muscles

Analysis of muscle fibre input dynamics using amyog: GFP transgenic trout model

Molecular Regulation and Rejuvenation of Muscle Stem (Satellite) Cell Aging

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