Skeletal muscle regeneration and impact of aging and nutrition

Domingues-Faria, Carla; Vasson, Marie‐Paule; Goncalves-Mendès, Nicolas; Boirie‌, Yves; Walrand, Stéphane

doi:10.1016/j.arr.2015.12.004

Cited by 114 publications

(109 citation statements)

References 169 publications

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“…In humans, sarcopenia is a common feature of aging that involves the accumulation of dysfunctional mitochondria and associated deterioration of muscle fiber cells themselves, in combination with infiltration of adipocytes and inflammatory immune cells52. In addition, an impaired ability of muscle stem cells to generate new myocytes may be impaired with aging and more so in sarcopenia53. All cells that comprise C. elegans pharyngeal muscles are postmitotic muscle cells.…”

Section: Discussionmentioning

confidence: 99%

Tomatidine enhances lifespan and healthspan in C. elegans through mitophagy induction via the SKN-1/Nrf2 pathway

Fang

Waltz

Kassahun

et al. 2017

Sci Rep

124

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Aging is a major international concern that brings formidable socioeconomic and healthcare challenges. Small molecules capable of improving the health of older individuals are being explored. Small molecules that enhance cellular stress resistance are a promising avenue to alleviate declines seen in human aging. Tomatidine, a natural compound abundant in unripe tomatoes, inhibits age-related skeletal muscle atrophy in mice. Here we show that tomatidine extends lifespan and healthspan in C. elegans, an animal model of aging which shares many major longevity pathways with mammals. Tomatidine improves many C. elegans behaviors related to healthspan and muscle health, including increased pharyngeal pumping, swimming movement, and reduced percentage of severely damaged muscle cells. Microarray, imaging, and behavioral analyses reveal that tomatidine maintains mitochondrial homeostasis by modulating mitochondrial biogenesis and PINK-1/DCT-1-dependent mitophagy. Mechanistically, tomatidine induces mitochondrial hormesis by mildly inducing ROS production, which in turn activates the SKN-1/Nrf2 pathway and possibly other cellular antioxidant response pathways, followed by increased mitophagy. This mechanism occurs in C. elegans, primary rat neurons, and human cells. Our data suggest that tomatidine may delay some physiological aspects of aging, and points to new approaches for pharmacological interventions for diseases of aging.

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Section: Discussionmentioning

confidence: 99%

Tomatidine enhances lifespan and healthspan in C. elegans through mitophagy induction via the SKN-1/Nrf2 pathway

Fang

Waltz

Kassahun

et al. 2017

Sci Rep

124

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“…However, a number of pathological conditions that may affect the innervation and distribution of nAChRs can lead to a reduction in the safety mechanism and result in the impairment of neuromuscular transmission (Wood and Slater, 2001). Injured peripheral nerves and skeletal muscles have a remarkable ability for tissue regeneration (Scheib and Hoke, 2013; Domingues-Faria et al, 2016), and regeneration of functional NMJs occurs after NMJ injury (McMahan et al, 1980; Darabid et al, 2014). Although, regenerated NMJs are mainly formed at original synaptic sites of the skeletal muscle (McMahan et al, 1980), growing evidence demonstrates that NMJs are also formed on regenerated axons and muscle fibers (Slater, 1982; Slater and Allen, 1985; Ijkema-Paassen et al, 2002; Nishizawa et al, 2003; Li and Thompson, 2011; Grumbles et al, 2012; Kang and Lichtman, 2013).…”

Section: Introductionmentioning

confidence: 99%

Morphological Regeneration and Functional Recovery of Neuromuscular Junctions after Tourniquet-Induced Injuries in Mouse Hindlimb

Zhang

Corrick

et al. 2017

Front. Physiol.

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Tourniquet application and its subsequent release cause serious injuries to the skeletal muscle, nerve, and neuromuscular junction (NMJ) due to mechanical compression and ischemia-reperfusion (IR). Monitoring structural and functional repair of the NMJ, nerve, and skeletal muscle after tourniquet-induced injuries is beneficial in exploring potential cellular and molecular mechanisms responsible for tourniquet-induced injuries, and for establishing effective therapeutic interventions. Here, we observed long-term morphological and functional changes of the NMJ in a murine model of tourniquet-induced hindlimb injuries. Unilateral hindlimbs of C57/BL6 mice were subjected to 3 h of tourniquet by placing an orthodontic rubber band, followed by varied periods of tourniquet release (1 day, 3 days, 1 week, 2 weeks, 4 weeks, and 6 weeks). NMJ morphology in the gastrocnemius muscle was imaged, and the endplate potential (EPP) was recorded to evaluate NMJ function. In NMJs, nicotinic acetylcholine receptor (nAChR) clusters normally displayed an intact, pretzel-like shape, and all nAChR clusters were innervated (100%) by motor nerve terminals. During 3 h of tourniquet application and varied periods of tourniquet release, NMJs in the gastrocnemius muscle were characterized by morphological and functional changes. At 1 day and 3 days of tourniquet release, nAChR clusters retained normal, pretzel-like shapes, whereas motor nerve terminals were completely destroyed and no EPPs recorded. From 1 to 6 weeks of tourniquet release, motor nerve terminals gradually regenerated, even reaching that seen in sham mice, whereas nAChR clusters were gradually fragmented with prolongation of tourniquet release. Additionally, the amplitude of EPPs gradually increased with prolongation of tourniquet release. However, even at 6 weeks after tourniquet release, the amplitude of EPPs did not restore to the level seen in sham mice (13.9 ± 1.1 mV, p < 0.05 vs. sham mice, 29.8 ± 1.0 mV). The data suggest that tourniquet application and subsequent release impair the structure and function of NMJs. Morphological change in motor nerve terminals is faster than in nAChR clusters in NMJs. Slow restoration of fragmented nAChR clusters possibly dampens neuromuscular transmission during the long phase following tourniquet release.

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“…The quality, amount and caloric value of food, as well as eating habits are all important factors influencing the overall health status (5). In society, different social and economic conditions result in social inequalities in the area of nutrition, which in turn lead to inequalities in health (6).…”

Section: Introductionmentioning

confidence: 99%

Risk Factors for Malnutrition in Seniors Aged 75+ Living in Home Environment in Selected Regions of the Czech Republic

Brabcová¹,

Trešlová²,

Bártlová³

et al. 2016

Cent Eur J Public Health

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SUMMARYBackground and Aim: Nutrition is an important social determinant of health that influences the ageing process. The aim of this study was to evaluate the nutritional condition of a group of seniors and identify the bio-psycho-social factors that increase the risk of malnutrition.Methods: The research was conducted using a quantitative method. The standardised scales Mini Nutritional Assessment -Short Form (MNA -SF) and the Geriatric depression scale (GDS-5) were used to evaluate the nutritional condition and tendency towards depression of the tested group. This group consisted of seniors aged 75 and above living in home environment in the České Budějovice region. The group was comprised of 320 seniors, 115 men (35.9%) and 205 women (64.1%), which corresponds to the composition of the population in the chosen region of the Czech Republic. Statistical data analysis was conducted using SASD 1.4.10 and SPSS 15.0 programs. Pearson's chi-squared test (χ 2 ) and Cramér's V were chosen for statistical testing. The significance level was set at 5%.Results: The average BMI value of the seniors was 26.2 kg/m 2 (overweight). This value decreased with age. More than one third of the respondents were evaluated as being at risk of malnutrition (36.3%). Unintended weight loss was determined as the strongest risk factor of malnutrition. Seniors who had lowered their food intake stated unintended weight loss 10 times more often than respondents with no noticeable reduction in food intake. Seniors who showed signs of depression indicated weight loss three and a half times more often than respondents without depression. Meanwhile acute illness increased the risk by three times. Depression was found to be the cause and also the consequence of malnutrition.Conclusion: Despite the high prevalence of overweight and obesity, a large proportion of the respondents were running the risk of malnutrition. It was concluded that the strongest risk factors for malnutrition in the respondents were unintended weight loss, depression and lowered food intake. Compared to biological factors, social and economic factors were less significant in causing malnutrition in seniors.

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Skeletal muscle regeneration and impact of aging and nutrition

Cited by 114 publications

References 169 publications

Tomatidine enhances lifespan and healthspan in C. elegans through mitophagy induction via the SKN-1/Nrf2 pathway

Tomatidine enhances lifespan and healthspan in C. elegans through mitophagy induction via the SKN-1/Nrf2 pathway

Morphological Regeneration and Functional Recovery of Neuromuscular Junctions after Tourniquet-Induced Injuries in Mouse Hindlimb

Risk Factors for Malnutrition in Seniors Aged 75+ Living in Home Environment in Selected Regions of the Czech Republic

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