Introduction to the Special Issue “Skeletal Muscle Atrophy: Mechanisms at a Cellular Level” (original) (raw)
Related papers
The molecular basis of skeletal muscle atrophy
American Journal of Physiology-Cell Physiology, 2004
Skeletal muscle atrophy attributable to muscular inactivity has significant adverse functional consequences. While the initiating physiological event leading to atrophy seems to be the loss of muscle tension and a good deal of the physiology of muscle atrophy has been characterized, little is known about the triggers or the molecular signaling events underlying this process. Decreases in protein synthesis and increases in protein degradation both have been shown to contribute to muscle protein loss due to disuse, and recent work has delineated elements of both synthetic and proteolytic processes underlying muscle atrophy. It is also becoming evident that interactions among known proteolytic pathways (ubiquitin-proteasome, lysosomal, and calpain) are involved in muscle proteolysis during atrophy. Factors such as TNF-α, glucocorticoids, myostatin, and reactive oxygen species can induce muscle protein loss under specified conditions. Also, it is now apparent that the transcription fact...
Mechanisms of muscle atrophy and hypertrophy: implications in health and disease
Nature Communications, 2021
Skeletal muscle is the protein reservoir of our body and an important regulator of glucose and lipid homeostasis. Consequently, the growth or the loss of muscle mass can influence general metabolism, locomotion, eating and respiration. Therefore, it is not surprising that excessive muscle loss is a bad prognostic index of a variety of diseases ranging from cancer, organ failure, infections and unhealthy ageing. Muscle function is influenced by different quality systems that regulate the function of contractile proteins and organelles. These systems are controlled by transcriptional dependent programs that adapt muscle cells to environmental and nutritional clues. Mechanical, oxidative, nutritional and energy stresses, as well as growth factors or cytokines modulate signaling pathways that, ultimately, converge on protein and organelle turnover. Novel insights that control and orchestrate such complex network are continuously emerging and will be summarized in this review. Understanding the mechanisms that control muscle mass will provide therapeutic targets for the treatment of muscle loss in inherited and non hereditary diseases and for the improvement of the quality of life during ageing.
Regulation of skeletal muscle atrophy
The Journal of Physical Fitness and Sports Medicine, 2013
Skeletal muscle atrophy can result from prolonged periods of skeletal muscle inactivity due to bed rest, denervation, or unloading. Such unloading-associated atrophy of skeletal muscle is characterized by both an increase in protein degradation and a decrease in protein synthesis. Successful treatments for skeletal muscle atrophy could either block protein degradation pathways activated during atrophy, or stimulate protein synthesis pathways induced during skeletal muscle hypertrophy. In this review, we mainly focus on the Insulin-like growth factor 1 (IGF-1)/Insulin receptor substrate 1 (IRS-1) pathway in muscle, because there is increasing evidence indicating that inhibition of this pathway in muscle is involved in the progression of disuse atrophy. We also focus on the signaling pathways that control skeletal muscle atrophy, including muscle atrophy-associated ubiqitin ligases such as Cbl-b, muscle RING finger 1 (MuRF1), and muscle atrophy F-box (MAFbx)/atrogin-1.
Cellular and molecular mechanisms of muscle atrophy
Disease Models & Mechanisms, 2012
Skeletal muscle is a plastic organ that is maintained by multiple pathways regulating cell and protein turnover. During muscle atrophy, proteolytic systems are activated, and contractile proteins and organelles are removed, resulting in the shrinkage of muscle fibers. Excessive loss of muscle mass is associated with poor prognosis in several diseases, including myopathies and muscular dystrophies, as well as in systemic disorders such as cancer, diabetes, sepsis and heart failure. Muscle loss also occurs during aging. In this paper, we review the key mechanisms that regulate the turnover of contractile proteins and organelles in muscle tissue, and discuss how impairments in these mechanisms can contribute to muscle atrophy. We also discuss how protein synthesis and degradation are coordinately regulated by signaling pathways that are influenced by mechanical stress, physical activity, and the availability of nutrients and growth factors. Understanding how these pathways regulate mus...
Review Article: Mechanisms and Strategies to Counter Muscle Atrophy
The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 2003
Skeletal muscle size is modulated by a number of factors, including muscle load, utilization, and regenerative capacity. Surprisingly, actions that can promote muscle growth do not necessarily prevent the loss of muscle mass, or atrophy. This suggests that divergent mechanisms are important for the maintenance of muscle mass in different contexts. In acute atrophy, muscles rapidly lose mass when load is lacking, and this response seems to involve active elimination of myonuclei. In contrast, chronic atrophy, such as loss of muscle mass related to aging, is associated with impairments in muscle repair. In this review, two contexts in which muscle mass is lost are explored to determine if similar processes are involved.
American journal of physiology. Endocrinology and metabolism, 2016
Muscle wasting resulting wholly or in part from disuse represents a serious medical complication, which when prolonged, can increase morbidity and mortality. Although much knowledge has been gained over the past half century, the underlying etiology by which disuse alters muscle proteostasis remains enigmatic. Multidisciplinary and novel methodologies are needed to fill gaps and overcome barriers to improved patient care. The present review highlights seminal concepts from a symposium at Experimental Biology 2016. These proceedings focus on the: (1) role of insulin resistance in mediating disuse-induced changes in muscle protein synthesis (MPS) and breakdown (MPB), as well as cross-talk between carbohydrate and protein metabolism; (2) the relative importance of MPS/MPB in mediating involuntary muscle loss in humans and animals; (3) interpretative limitations associated with MPS/MPB "markers" e.g. MuRF1/MAFbx mRNA; and finally, (4) how OMIC technologies can be leveraged to ...
Cells
Skeletal muscle tissue has the important function of supporting and defending the organism. It is the largest apparatus in the human body, and its function is important for contraction and movements. In addition, it is involved in the regulation of protein synthesis and degradation. In fact, inhibition of protein synthesis and/or activation of catabolism determines a pathological condition called muscle atrophy. Muscle atrophy is a reduction in muscle mass resulting in a partial or complete loss of function. It has been established that many physiopathological conditions can cause a reduction in muscle mass. Nevertheless, it is not well known the molecular mechanisms and signaling processes causing this dramatic event. There are multiple concomitant processes involved in muscle atrophy. In fact, the gene transcription of some factors, oxidative stress mechanisms, and the alteration of ion transport through specific ion channels may contribute to muscle function impairment. In this r...
Metabolic Remodeling in Skeletal Muscle Atrophy as a Therapeutic Target
Metabolites, 2021
Skeletal muscle is a highly responsive tissue, able to remodel its size and metabolism in response to external demand. Muscle fibers can vary from fast glycolytic to slow oxidative, and their frequency in a specific muscle is tightly regulated by fiber maturation, innervation, or external causes. Atrophic conditions, including aging, amyotrophic lateral sclerosis, and cancer-induced cachexia, differ in the causative factors and molecular signaling leading to muscle wasting; nevertheless, all of these conditions are characterized by metabolic remodeling, which contributes to the pathological progression of muscle atrophy. Here, we discuss how changes in muscle metabolism can be used as a therapeutic target and review the evidence in support of nutritional interventions and/or physical exercise as tools for counteracting muscle wasting in atrophic conditions.
Adaptations in Skeletal Muscle Disuse or Decreased-Use Atrophy
American Journal of Physical Medicine & Rehabilitation, 2002
Those factors that seem to play some role in inducing adaptations of skeletal muscle in vivo are discussed. The role of myogenesis in maintaining and repairing muscle during atrophic and hypertrophic states is discussed, including pointing out that the modulation of myonuclear number is one means of adapting to varying chronic levels of neuromuscular activity. Finally, we point out the potential consequences of muscle atrophy on the control of movement and the susceptibility to fatigue.