Lack of physical activity due to an injury or illness, poor nutrition, genetics, and certain medical conditions can all contribute to muscle atrophy. Muscle atrophy can occur after long periods of inactivity. If a muscle does not get any use, the body will eventually break it down to conserve energy. Muscle atrophy that develops due to inactivity can occur if a person remains immobile while they recover from an illness or injury. Getting regular exercise and trying physical therapy may reverse this form of muscle atrophy.
People can treat muscle atrophy by making certain lifestyle changes, trying physical therapy, or undergoing surgery. Poor nutrition can give rise to numerous health conditions, including muscle atrophy. Specifically, the International Osteoporosis Foundation warn that diets low in lean protein, fruits, and vegetables can lead to reductions in muscle mass. Cachexia is a complex metabolic condition that causes extreme weight loss and muscle atrophy.
Cachexia can develop as a symptom of another underlying condition, such as cancer, HIV , or multiple sclerosis MS. People who have cachexia may experience a significant loss of appetite or unintentional weight loss despite consuming a large number of calories. As a person gets older, their body produces fewer proteins that promote muscle growth. This reduction of available protein causes the muscle cells to shrink, resulting in a condition called sarcopenia.
A loss of muscle mass may be an inevitable result of the natural aging process. Spinal muscular atrophy SMA is a genetic disorder that causes a loss of motor nerve cells and muscle atrophy. Muscular dystrophy refers to a group of progressive conditions that cause loss of muscle mass and weakness. Muscular dystrophy occurs when one of the genes involved in protein production mutates.
A person can inherit genetic mutations, but many occur naturally as the embryo develops. This type of muscle atrophy tends to occur more suddenly than physiologic atrophy. Although people can adapt to muscle atrophy, even minor muscle atrophy causes some loss of movement or strength. An exercise program may help treat muscle atrophy. Exercises may include ones done in a swimming pool to reduce the muscle workload, and other types of rehabilitation.
Your health care provider can tell you more about this. People who cannot actively move one or more joints can do exercises using braces or splints. Call your provider for an appointment if you have unexplained or long-term muscle loss. You can often see this when you compare one hand, arm, or leg to the other. The provider will perform a physical examination and ask about your medical history and symptoms, including:.
The provider will look at your arms and legs and measure muscle size. This may help determine which nerves are affected. Treatment may include physical therapy, ultrasound therapy and, in some cases, surgery to correct a contracture. Musculoskeletal system. Seidel's Guide to Physical Examination. Journal List Dis Model Mech v. Dis Model Mech. Paolo Bonaldo 1 and Marco Sandri 1, 2. Author information Copyright and License information Disclaimer.
Published by The Company of Biologists Ltd. This article has been cited by other articles in PMC. Abstract Skeletal muscle is a plastic organ that is maintained by multiple pathways regulating cell and protein turnover. Introduction Muscles are the largest protein reservoir in the body. The ubiquitin-proteasome system In muscle, the ubiquitin-proteasome system is required to remove sarcomeric proteins upon changes in muscle activity.
Open in a separate window. Table 1. The autophagy-lysosome system Autophagy plays a crucial role in the turnover of cell components both in constitutive conditions and in response to various stimuli, such as cellular stress, nutrient deprivation, amino acid starvation and cytokines Mizushima et al. Signaling pathways regulating muscle atrophy Many recent findings have highlighted a complex scenario whereby an intricate network of signaling pathways regulates the size of myofibers and the contractile performance of muscle.
Glucocorticoid-induced muscle atrophy and the control of protein homeostasis Glucocorticoid levels are increased in many pathological conditions associated with muscle loss. Therapeutic perspectives for counteracting muscle atrophy The mechanisms controlling muscle mass have attracted increasing interest in the scientific community because increased understanding of these can potentially help to tackle various clinical problems, including aging, the prognosis of many diseases, quality of life and sports medicine.
Acknowledgments We apologize to colleagues whose studies were not cited owing to space limitations. Chaperone-assisted selective autophagy is essential for muscle maintenance. Muscle sparing in muscle RING finger 1 null mice: response to synthetic glucocorticoids. The E3 ubiquitin ligase specificity subunit ASB2beta is a novel regulator of muscle differentiation that targets filamin B to proteasomal degradation.
Cell Death Differ. Skeletal muscle-specific ablation of raptor, but not of rictor, causes metabolic changes and results in muscle dystrophy. Cell Metab. Dysfunction of mitochondria and sarcoplasmic reticulum in the pathogenesis of collagen VI muscular dystrophies. Posttranslational modifications control FoxO3 activity during denervation.
Inducible activation of Akt increases skeletal muscle mass and force without satellite cell activation. Identification of ubiquitin ligases required for skeletal muscle atrophy. Cell Biol. Selective expression of Cre recombinase in skeletal muscle fibers. Peroxisome proliferator-activated receptor gamma coactivator 1alpha or 1beta overexpression inhibits muscle protein degradation, induction of ubiquitin ligases, and disuse atrophy. The FoxO code. The proteasome inhibitor MG reduces immobilization-induced skeletal muscle atrophy in mice.
BMC Musculoskelet. Bclassociated autophagy regulator Naf-1 required for maintenance of skeletal muscle. A mutation creating a potential illegitimate microRNA target site in the myostatin gene affects muscularity in sheep.
During muscle atrophy, thick, but not thin, filament components are degraded by MuRF1-dependent ubiquitylation. Ubiquitylation by Trim32 causes coupled loss of desmin, Z-bands, and thin filaments in muscle atrophy. USP19 is a ubiquitin-specific protease regulated in rat skeletal muscle during catabolic states. Gene Ther. The translation regulatory subunit eIF3f controls the kinase-dependent mTOR signaling required for muscle differentiation and hypertrophy in mouse.
Autophagy and aging: keeping that old broom working. Trends Genet. Tumor necrosis factor alpha produces insulin resistance in skeletal muscle by activation of inhibitor kappaB kinase in a p38 MAPK-dependent manner. Identification of cathepsin L as a differentially expressed message associated with skeletal muscle wasting. Ectopic expression of myostatin induces atrophy of adult skeletal muscle by decreasing muscle gene expression.
Muscle-specific inactivation of the IGF -I receptor induces compensatory hyperplasia in skeletal muscle. Myosin accumulation and striated muscle myopathy result from the loss of muscle RING finger 1 and 3. Dysfunction of endocytic and autophagic pathways in a lysosomal storage disease. Autophagy and lysosomes in Pompe disease.
Role of different proteolytic systems in the degradation of muscle proteins during denervation atrophy. Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy. A FoxO-Smad synexpression group in human keratinocytes. Modulating skeletal muscle mass by postnatal, muscle-specific inactivation of the myostatin gene. Autophagy is defective in collagen VI muscular dystrophies, and its reactivation rescues myofiber degeneration.
Autophagy induction rescues muscular dystrophy. Physical exercise stimulates autophagy in normal skeletal muscles but is detrimental for collagen VI-deficient muscles. Microtubule-associated protein 1 light chain 3 LC3 interacts with Bnip3 protein to selectively remove endoplasmic reticulum and mitochondria via autophagy.
Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice. Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis.
A central role for JNK in obesity and insulin resistance. A novel ubiquitin-binding protein ZNF functioning in muscle atrophy. EMBO J. Dynamic FoxO transcription factors. Cell Sci. Disruption of either the Nfkb1 or the Bcl3 gene inhibits skeletal muscle atrophy. Prevention of muscle disuse atrophy by MG proteasome inhibitor. Role for IkappaBalpha, but not c-Rel, in skeletal muscle atrophy. A role for NBR1 in autophagosomal degradation of ubiquitinated substrates.
Rapamycin inhibits the growth and muscle-sparing effects of clenbuterol. Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes.
Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice. Chaperone-mediated autophagy in health and disease. FEBS Lett. Satellite cell senescence underlies myopathy in a mouse model of limb-girdle muscular dystrophy 2H. Conditional activation of akt in adult skeletal muscle induces rapid hypertrophy. Protein degradation by the ubiquitin-proteasome pathway in normal and disease states. Regulation of muscle mass by myostatin.
Cell Dev. Quadrupling muscle mass in mice by targeting TGF-beta signaling pathways. Myostatin and the control of skeletal muscle mass. Regulation of myostatin activity and muscle growth. Regulation of muscle protein degradation: coordinated control of apoptotic and ubiquitin-proteasome systems by phosphatidylinositol 3 kinase. Sestrin as a feedback inhibitor of TOR that prevents age-related pathologies. Rapid disuse atrophy of diaphragm fibers in mechanically ventilated humans.
Effect of RNA oligonucleotide targeting Foxo-1 on muscle growth in normal and cancer cachexia mice. Cancer Gene Ther. Myostatin induces degradation of sarcomeric proteins through a Smad3 signaling mechanism during skeletal muscle wasting. Lysosomal myopathies: an excessive build-up in autophagosomes is too much to handle. FoxO3 controls autophagy in skeletal muscle in vivo. Autophagy inhibition induces atrophy and myopathy in adult skeletal muscles.
Autophagy is required to maintain muscle mass. Smad transcription factors. Genes Dev. Effective fiber hypertrophy in satellite cell-depleted skeletal muscle. Myostatin induces cachexia by activating the ubiquitin proteolytic system through an NF-kappaB-independent, FoxO1-dependent mechanism. Double muscling in cattle due to mutations in the myostatin gene. Regulation of skeletal muscle mass in mice by a new TGF-beta superfamily member. Role of glucocorticoids in the molecular regulation of muscle wasting.
Care Med. S6 kinase inactivation impairs growth and translational target phosphorylation in muscle cells maintaining proper regulation of protein turnover. In vivo analysis of autophagy in response to nutrient starvation using transgenic mice expressing a fluorescent autophagosome marker. Autophagy fights disease through cellular self-digestion. Insulin and insulin-like growth factor I.
Effects on protein synthesis in isolated muscles from lean and goldthioglucose-obese mice. Histone deacetylases 1 and 2 regulate autophagy flux and skeletal muscle homeostasis in mice. Myostatin regulates cardiomyocyte growth through modulation of Akt signaling. Targeted ablation of IKK2 improves skeletal muscle strength, maintains mass, and promotes regeneration.
Localized Igf-1 transgene expression sustains hypertrophy and regeneration in senescent skeletal muscle. AMPK activation stimulates myofibrillar protein degradation and expression of atrophy-related ubiquitin ligases by increasing FOXO transcription factors in C2C12 myotubes.
Redox Signal. Nix is a selective autophagy receptor for mitochondrial clearance. EMBO Rep. Unexpected cardiotoxicity in haematological bortezomib treated patients. FoxOs are lineage-restricted redundant tumor suppressors and regulate endothelial cell homeostasis. Autophagic degradation of nuclear components in mammalian cells. Targeted ablation of TRAF6 inhibits skeletal muscle wasting in mice. The E3 ubiquitin ligase TRAF6 intercedes in starvation-induced skeletal muscle atrophy through multiple mechanisms.
Dwarfism, impaired skin development, skeletal muscle atrophy, delayed bone development, and impeded adipogenesis in mice lacking Akt1 and Akt2. DHPR alpha1S subunit controls skeletal muscle mass and morphogenesis. Suppression of autophagy in skeletal muscle uncovers the accumulation of ubiquitinated proteins and their potential role in muscle damage in Pompe disease.
JunB transcription factor maintains skeletal muscle mass and promotes hypertrophy. Inhibition of FoxO transcriptional activity prevents muscle fiber atrophy during cachexia and induces hypertrophy. Lower skeletal muscle mass in male transgenic mice with muscle-specific overexpression of myostatin. Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy. Mitochondrial biogenesis and fragmentation as regulators of muscle protein degradation.
Mitochondrial fission and remodelling contributes to muscle atrophy. IGF-I stimulates muscle growth by suppressing protein breakdown and expression of atrophy-related ubiquitin ligases, atrogin-1 and MuRF1. Rapid disuse and denervation atrophy involve transcriptional changes similar to those of muscle wasting during systemic diseases. Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy.
PGC-1alpha protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription. Molecular and cellular determinants of skeletal muscle atrophy and hypertrophy. STKE , re Smad2 and 3 transcription factors control muscle mass in adulthood.
Cell Physiol. Mechanisms of glucocorticoid-induced myopathy. Studies on the effect of denervation in developing muscle.
0コメント