scholarly journals Changes in Redox Signaling in the Skeletal Muscle with Aging

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Péter Szentesi ◽  
László Csernoch ◽  
László Dux ◽  
Anikó Keller-Pintér
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Mass ◽  
Driving Forces ◽  
Force Production ◽  
Production Quality ◽  
Muscle Loss ◽  
Muscle Stem Cells ◽  
Age Related ◽  
And Function

Reduction in muscle strength with aging is due to both loss of muscle mass (quantity) and intrinsic force production (quality). Along with decreased functional capacity of the muscle, age-related muscle loss is associated with corresponding comorbidities and healthcare costs. Mitochondrial dysfunction and increased oxidative stress are the central driving forces for age-related skeletal muscle abnormalities. The increased oxidative stress in the aged muscle can lead to altered excitation-contraction coupling and calcium homeostasis. Furthermore, apoptosis-mediated fiber loss, atrophy of the remaining fibers, dysfunction of the satellite cells (muscle stem cells), and concomitant impaired muscle regeneration are also the consequences of increased oxidative stress, leading to a decrease in muscle mass, strength, and function of the aged muscle. Here we summarize the possible effects of oxidative stress in the aged muscle and the benefits of physical activity and antioxidant therapy.

scholarly journals NEUROMUSCULAR CHANGES WITH AGING AND SARCOPENIA

2018 ◽  
pp. 1-3
Author(s):  
B.C. Clark
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Function ◽  
Skeletal Muscle Mass ◽  
The Past ◽  
Conceptual Definition ◽  
Age Related ◽  
Per Se ◽  
Definition Of ◽  
And Function

Sarcopenia was originally conceptualized as the age-related loss of skeletal muscle mass. Over the ensuing decades, the conceptual definition of sarcopenia has changed to represent a condition in older adults that is characterized by declining muscle mass and function, with “function” most commonly conceived as muscle weakness and/or impaired physical performance (e.g., slow gait speed). Findings over the past 15-years, however, have demonstrated that changes in grip and leg extensor strength are not primarily due to muscle atrophy per se, and that to a large extent, are reflective of declines in the integrity of the nervous system. This article briefly summarizes findings relating to the complex neuromuscular mechanisms that contribute to reductions in muscle function associated with advancing age, and the implications of these findings on the development of effective therapies.

scholarly journals The Effect of MicroRNA-Mediated Exercise on Delaying Sarcopenia in Elderly Individuals

Dose-Response ◽  
2020 ◽  
Vol 18 (4) ◽  
pp. 155932582097454
Author(s):  
Wen-Qing Xie ◽  
Chen Men ◽  
Miao He ◽  
Yu-sheng Li ◽  
Shan Lv
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Fiber Type ◽  
Treatment Strategies ◽  
Cellular Level ◽  
Core Element ◽  
Muscle Stem Cells ◽  
Elderly Individuals ◽  
Activated State ◽  
And Function

Sarcopenia is often regarded as an early sign of weakness and is the core element of muscle weakness in elderly individuals. Sarcopenia is closely related to the reduction of exercise, and elderly individuals often suffer from decreased muscle mass and function due to a lack of exercise. At present, studies have confirmed that resistance and aerobic exercise are related to muscle mass, strength and fiber type and to the activation and proliferation of muscle stem cells (MuSCs). Increasing evidence shows that microRNAs (miRNAs) play an important role in exercise-related changes in the quantity, composition and function of skeletal muscle. At the cellular level, miRNAs have been shown to regulate the proliferation and differentiation of muscle cells. In addition, miRNAs are related to the composition and transformation of muscle fibers and involved in the transition of MuSCs from the resting state to the activated state. Therefore, exercise may delay sarcopenia in elderly individuals by regulating miRNAs in skeletal muscle. In future miRNA-focused treatment strategies, these studies will provide valuable information for the formulation of exercise methods and will provide useful and targeted exercise programs for elderly individuals with sarcopenia.

scholarly journals An investigation of p53 in skeletal muscle aging

2019 ◽  
Vol 127 (4) ◽  
pp. 1075-1084 ◽  
Author(s):  
Scott M. Ebert ◽  
Jason M. Dierdorff ◽  
David K. Meyerholz ◽  
Steven A. Bullard ◽  
Asma Al-Zougbi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Muscle Fibers ◽  
Skeletal Muscle Atrophy ◽  
P53 Expression ◽  
Skeletal Muscle Fibers ◽  
Age Related ◽  
Skeletal Muscle Aging ◽  
And Function

Age-related skeletal muscle atrophy is a very common and serious condition that remains poorly understood at the molecular level. Several lines of evidence have suggested that the tumor suppressor p53 may play a central, causative role in skeletal muscle aging, whereas other, apparently contradictory lines of evidence have suggested that p53 may be critical for normal skeletal muscle function. To help address these issues, we performed an aging study in male muscle-specific p53-knockout mice (p53 mKO mice), which have a lifelong absence of p53 expression in skeletal muscle fibers. We found that the absence of p53 expression in skeletal muscle fibers had no apparent deleterious or beneficial effects on skeletal muscle mass or function under basal conditions up to 6 mo of age, when mice are fully grown and exhibit peak muscle mass and function. Furthermore, at 22 and 25 mo of age, when age-related muscle weakness and atrophy are clearly evident in mice, p53 mKO mice demonstrated no improvement or worsening of skeletal muscle mass or function relative to littermate control mice. At advanced ages, p53 mKO mice began to die prematurely and had an increased incidence of osteosarcoma, precluding analyses of muscle mass and function in very old p53 mKO mice. In light of these results, we conclude that p53 expression in skeletal muscle fibers has minimal if any direct, cell autonomous effect on basal or age-related changes in skeletal muscle mass and function up to at least 22 mo of age. NEW & NOTEWORTHY Previous studies implicated the transcriptional regulator p53 as a potential mediator of age-related skeletal muscle weakness and atrophy. We tested this hypothesis by investigating the effect of aging in muscle-specific p53-knockout mice. Our results strongly suggest that p53 activity within skeletal muscle fibers is not required for age-related skeletal muscle atrophy or weakness.

scholarly journals MICU3 regulates mitochondrial Ca2+-dependent antioxidant response in skeletal muscle aging

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Yun-Fei Yang ◽  
Wu Yang ◽  
Zhi-Yin Liao ◽  
Yong-Xin Wu ◽  
Zhen Fan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Calcium Uptake ◽  
Mitochondrial Calcium ◽  
Muscle Aging ◽  
Skeletal Muscle Aging ◽  
And Function ◽  
Mitochondrial Calcium Uptake

AbstractAge-related loss of skeletal muscle mass and function, termed sarcopenia, could impair the quality of life in the elderly. The mechanisms involved in skeletal muscle aging are intricate and largely unknown. However, more and more evidence demonstrated that mitochondrial dysfunction and apoptosis also play an important role in skeletal muscle aging. Recent studies have shown that mitochondrial calcium uniporter (MCU)-mediated mitochondrial calcium affects skeletal muscle mass and function by affecting mitochondrial function. During aging, we observed downregulated expression of mitochondrial calcium uptake family member3 (MICU3) in skeletal muscle, a regulator of MCU, which resulted in a significant reduction in mitochondrial calcium uptake. However, the role of MICU3 in skeletal muscle aging remains poorly understood. Therefore, we investigated the effect of MICU3 on the skeletal muscle of aged mice and senescent C2C12 cells induced by d-gal. Downregulation of MICU3 was associated with decreased myogenesis but increased oxidative stress and apoptosis. Reconstitution of MICU3 enhanced antioxidants, prevented the accumulation of mitochondrial ROS, decreased apoptosis, and increased myogenesis. These findings indicate that MICU3 might promote mitochondrial Ca2+ homeostasis and function, attenuate oxidative stress and apoptosis, and restore skeletal muscle mass and function. Therefore, MICU3 may be a potential therapeutic target in skeletal muscle aging.

scholarly journals Nutrition and microRNAs: Novel Insights to Fight Sarcopenia

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 951
Author(s):  
Alessandra Barbiera ◽  
Laura Pelosi ◽  
Gigliola Sica ◽  
Bianca Maria Scicchitano
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Molecular Mechanisms ◽  
Muscle Protein ◽  
Low Grade ◽  
Protein Homeostasis ◽  
Dietary Interventions ◽  
Physiological Processes ◽  
Age Related ◽  
And Function

Sarcopenia is a progressive age-related loss of skeletal muscle mass and strength, which may result in increased physical frailty and a higher risk of adverse events. Low-grade systemic inflammation, loss of muscle protein homeostasis, mitochondrial dysfunction, and reduced number and function of satellite cells seem to be the key points for the induction of muscle wasting, contributing to the pathophysiological mechanisms of sarcopenia. While a range of genetic, hormonal, and environmental factors has been reported to contribute to the onset of sarcopenia, dietary interventions targeting protein or antioxidant intake may have a positive effect in increasing muscle mass and strength, regulating protein homeostasis, oxidative reaction, and cell autophagy, thus providing a cellular lifespan extension. MicroRNAs (miRNAs) are endogenous small non-coding RNAs, which control gene expression in different tissues. In skeletal muscle, a range of miRNAs, named myomiRNAs, are involved in many physiological processes, such as growth, development, and maintenance of muscle mass and function. This review aims to present and to discuss some of the most relevant molecular mechanisms related to the pathophysiological effect of sarcopenia. Besides, we explored the role of nutrition as a possible way to counteract the loss of muscle mass and function associated with ageing, with special attention paid to nutrient-dependent miRNAs regulation. This review will provide important information to better understand sarcopenia and, thus, to facilitate research and therapeutic strategies to counteract the pathophysiological effect of ageing.

scholarly journals Recent advances and future avenues in understanding the role of adipose tissue cross talk in mediating skeletal muscle mass and function with ageing

GeroScience ◽  
2021 ◽  
Author(s):  
Andrew Wilhelmsen ◽  
Kostas Tsintzas ◽  
Simon W. Jones
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Muscle Mass ◽  
Extracellular Vesicles ◽  
Cross Talk ◽  
Skeletal Muscle Mass ◽  
Activity Level ◽  
Age Related ◽  
And Function

AbstractSarcopenia, broadly defined as the age-related decline in skeletal muscle mass, quality, and function, is associated with chronic low-grade inflammation and an increased likelihood of adverse health outcomes. The regulation of skeletal muscle mass with ageing is complex and necessitates a delicate balance between muscle protein synthesis and degradation. The secretion and transfer of cytokines, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), both discretely and within extracellular vesicles, have emerged as important communication channels between tissues. Some of these factors have been implicated in regulating skeletal muscle mass, function, and pathologies and may be perturbed by excessive adiposity. Indeed, adipose tissue participates in a broad spectrum of inter-organ communication and obesity promotes the accumulation of macrophages, cellular senescence, and the production and secretion of pro-inflammatory factors. Pertinently, age-related sarcopenia has been reported to be more prevalent in obesity; however, such effects are confounded by comorbidities and physical activity level. In this review, we provide evidence that adiposity may exacerbate age-related sarcopenia and outline some emerging concepts of adipose-skeletal muscle communication including the secretion and processing of novel myokines and adipokines and the role of extracellular vesicles in mediating inter-tissue cross talk via lncRNAs and miRNAs in the context of sarcopenia, ageing, and obesity. Further research using advances in proteomics, transcriptomics, and techniques to investigate extracellular vesicles, with an emphasis on translational, longitudinal human studies, is required to better understand the physiological significance of these factors, the impact of obesity upon them, and their potential as therapeutic targets in combating muscle wasting.

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