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Journal articles on the topic 'Atrophy signaling pathways'

Author: Grafiati

Published: 18 April 2022

Last updated: 30 July 2025

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1

Hulmi, Juha J., Mika Silvennoinen, Maarit Lehti, Riikka Kivelä, and Heikki Kainulainen. "Altered REDD1, myostatin, and Akt/mTOR/FoxO/MAPK signaling in streptozotocin-induced diabetic muscle atrophy." American Journal of Physiology-Endocrinology and Metabolism 302, no. 3 (2012): E307—E315. http://dx.doi.org/10.1152/ajpendo.00398.2011.

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Type 1 diabetes, if poorly controlled, leads to skeletal muscle atrophy, decreasing the quality of life. We aimed to search highly responsive genes in diabetic muscle atrophy in a common diabetes model and to further characterize associated signaling pathways. Mice were killed 1, 3, or 5 wk after streptozotocin or control. Gene expression of calf muscles was analyzed using microarray and protein signaling with Western blotting. We identified translational repressor protein REDD1 (regulated in development and DNA damage responses) that increased seven- to eightfold and was associated with muscl

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Powers, Scott K., Andreas N. Kavazis, and Joseph M. McClung. "Oxidative stress and disuse muscle atrophy." Journal of Applied Physiology 102, no. 6 (2007): 2389–97. http://dx.doi.org/10.1152/japplphysiol.01202.2006.

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Skeletal muscle inactivity is associated with a loss of muscle protein and reduced force-generating capacity. This disuse-induced muscle atrophy results from both increased proteolysis and decreased protein synthesis. Investigations of the cell signaling pathways that regulate disuse muscle atrophy have increased our understanding of this complex process. Emerging evidence implicates oxidative stress as a key regulator of cell signaling pathways, leading to increased proteolysis and muscle atrophy during periods of prolonged disuse. This review will discuss the role of reactive oxygen species

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Clavel, Stephan, Sandrine Siffroi-Fernandez, Anne Sophie Coldefy, Kim Boulukos, Didier F. Pisani, and Benoît Dérijard. "Regulation of the Intracellular Localization of Foxo3a by Stress-Activated Protein Kinase Signaling Pathways in Skeletal Muscle Cells." Molecular and Cellular Biology 30, no. 2 (2009): 470–80. http://dx.doi.org/10.1128/mcb.00666-09.

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ABSTRACT Muscle atrophy is a debilitating process associated with many chronic wasting diseases, like cancer, diabetes, sepsis, and renal failure. Rapid loss of muscle mass occurs mainly through the activation of protein breakdown by the ubiquitin proteasome pathway. Foxo3a transcription factor is critical for muscle atrophy, since it activates the expression of ubiquitin ligase Atrogin-1. In several models of atrophy, inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway induces nuclear import of Foxo3a through an Akt-dependent process. This study aimed to identify sign

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4

Glass, David J. "Skeletal muscle hypertrophy and atrophy signaling pathways." International Journal of Biochemistry & Cell Biology 37, no. 10 (2005): 1974–84. http://dx.doi.org/10.1016/j.biocel.2005.04.018.

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Bodine, Sue C. "Edward F. Adolph Distinguished Lecture. Skeletal muscle atrophy: Multiple pathways leading to a common outcome." Journal of Applied Physiology 129, no. 2 (2020): 272–82. http://dx.doi.org/10.1152/japplphysiol.00381.2020.

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Skeletal muscle atrophy continues to be a serious consequence of many diseases and conditions for which there is no treatment. Our understanding of the mechanisms regulating skeletal muscle mass has improved considerably over the past two decades. For many years it was known that skeletal muscle atrophy resulted from an imbalance between protein synthesis and protein breakdown, with the net balance shifting toward protein breakdown. However, the molecular and cellular mechanisms underlying the increased breakdown of myofibrils was unknown. Over the past two decades, numerous reports have ident

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Mañas-García, Laura, Charlotte Denhard, Javier Mateu, Xavier Duran, Joaquim Gea, and Esther Barreiro. "Beneficial Effects of Resveratrol in Mouse Gastrocnemius: A Hint to Muscle Phenotype and Proteolysis." Cells 10, no. 9 (2021): 2436. http://dx.doi.org/10.3390/cells10092436.

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We hypothesized that the phenolic compound resveratrol mitigates muscle protein degradation and loss and improves muscle fiber cross-sectional area (CSA) in gastrocnemius of mice exposed to unloading (7dI). In gastrocnemius of mice (female C57BL/6J, 10 weeks) exposed to a seven-day period of hindlimb immobilization with/without resveratrol treatment, markers of muscle proteolysis (tyrosine release, systemic troponin-I), atrophy signaling pathways, and muscle phenotypic features and function were analyzed. In gastrocnemius of unloaded mice treated with resveratrol, body and muscle weight and fu

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Franch, Harold A., and S. Russ Price. "Molecular signaling pathways regulating muscle proteolysis during atrophy." Current Opinion in Clinical Nutrition and Metabolic Care 8, no. 3 (2005): 271–75. http://dx.doi.org/10.1097/01.mco.0000165005.01331.45.

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Yoshida, Tadashi, and Patrice Delafontaine. "Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy." Cells 9, no. 9 (2020): 1970. http://dx.doi.org/10.3390/cells9091970.

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Insulin-like growth factor-1 (IGF-1) is a key growth factor that regulates both anabolic and catabolic pathways in skeletal muscle. IGF-1 increases skeletal muscle protein synthesis via PI3K/Akt/mTOR and PI3K/Akt/GSK3β pathways. PI3K/Akt can also inhibit FoxOs and suppress transcription of E3 ubiquitin ligases that regulate ubiquitin proteasome system (UPS)-mediated protein degradation. Autophagy is likely inhibited by IGF-1 via mTOR and FoxO signaling, although the contribution of autophagy regulation in IGF-1-mediated inhibition of skeletal muscle atrophy remains to be determined. Evidence h

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Cussonneau, Laura, Christian Boyer, Charlotte Brun та ін. "Concurrent BMP Signaling Maintenance and TGF-β Signaling Inhibition Is a Hallmark of Natural Resistance to Muscle Atrophy in the Hibernating Bear". Cells 10, № 8 (2021): 1873. http://dx.doi.org/10.3390/cells10081873.

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Muscle atrophy arises from a multiplicity of physio-pathological situations and has very detrimental consequences for the whole body. Although knowledge of muscle atrophy mechanisms keeps growing, there is still no proven treatment to date. This study aimed at identifying new drivers for muscle atrophy resistance. We selected an innovative approach that compares muscle transcriptome between an original model of natural resistance to muscle atrophy, the hibernating brown bear, and a classical model of induced atrophy, the unloaded mouse. Using RNA sequencing, we identified 4415 differentially e

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10

Sandri, Marco. "Signaling in Muscle Atrophy and Hypertrophy." Physiology 23, no. 3 (2008): 160–70. http://dx.doi.org/10.1152/physiol.00041.2007.

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Muscle performance is influenced by turnover of contractile proteins. Production of new myofibrils and degradation of existing proteins is a delicate balance, which, depending on the condition, can promote muscle growth or loss. Protein synthesis and protein degradation are coordinately regulated by pathways that are influenced by mechanical stress, physical activity, availability of nutrients, and growth factors. Understanding the signaling that regulates muscle mass may provide potential therapeutic targets for the prevention and treatment of muscle wasting in metabolic and neuromuscular dis

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Kamal, Khaled Y., and Marina Trombetta-Lima. "Mechanotransduction and Skeletal Muscle Atrophy: The Interplay Between Focal Adhesions and Oxidative Stress." International Journal of Molecular Sciences 26, no. 6 (2025): 2802. https://doi.org/10.3390/ijms26062802.

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Mechanical unloading leads to profound musculoskeletal degeneration, muscle wasting, and weakness. Understanding the specific signaling pathways involved is essential for uncovering effective interventions. This review provides new perspectives on mechanotransduction pathways, focusing on the critical roles of focal adhesions (FAs) and oxidative stress in skeletal muscle atrophy under mechanical unloading. As pivotal mechanosensors, FAs integrate mechanical and biochemical signals to sustain muscle structural integrity. When disrupted, these complexes impair force transmission, activating prot

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Bilodeau, Philippe A., Erin S. Coyne, and Simon S. Wing. "The ubiquitin proteasome system in atrophying skeletal muscle: roles and regulation." American Journal of Physiology-Cell Physiology 311, no. 3 (2016): C392—C403. http://dx.doi.org/10.1152/ajpcell.00125.2016.

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Muscle atrophy complicates many diseases as well as aging, and its presence predicts both decreased quality of life and survival. Much work has been conducted to define the molecular mechanisms involved in maintaining protein homeostasis in muscle. To date, the ubiquitin proteasome system (UPS) has been shown to play an important role in mediating muscle wasting. In this review, we have collated the enzymes in the UPS whose roles in muscle wasting have been confirmed through loss-of-function studies. We have integrated information on their mechanisms of action to create a model of how they wor

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Kumagai, Hiroshi, Ana Raquel Coelho, Junxiang Wan, et al. "MOTS-c reduces myostatin and muscle atrophy signaling." American Journal of Physiology-Endocrinology and Metabolism 320, no. 4 (2021): E680—E690. http://dx.doi.org/10.1152/ajpendo.00275.2020.

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MOTS-c, a mitochondrial-derived peptide reduces high-fat-diet-induced muscle atrophy signaling by reducing myostatin expression. The CK2-PTEN-mTORC2-AKT-FOXO1 pathways play key roles in MOTS-c action on myostatin expression.

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Dupont, Erwan, Caroline Cieniewski-Bernard, Bruno Bastide, and Laurence Stevens. "Electrostimulation during hindlimb unloading modulates PI3K-AKT downstream targets without preventing soleus atrophy and restores slow phenotype through ERK." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 2 (2011): R408—R417. http://dx.doi.org/10.1152/ajpregu.00793.2009.

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Our aim was to analyze the role of phosphatidylinositol 3-kinase (PI3K)-AKT and MAPK signaling pathways in the regulation of muscle mass and slow-to-fast phenotype transition during hindlimb unloading (HU). For that purpose, we studied, in rat slow soleus and fast extensor digitorum longus muscles, the time course of anabolic PI3K-AKT-mammalian target of rapamycin, catabolic PI3K-AKT-forkhead box O (FOXO), and MAPK signaling pathway activation after 7, 14, and 28 days of HU. Moreover, we performed chronic low-frequency soleus electrostimulation during HU to maintain exclusively contractile phe

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Wang, Piao, Seok Yong Kang, Su Jin Kim, Yong-Ki Park, and Hyo Won Jung. "Monotropein Improves Dexamethasone-Induced Muscle Atrophy via the AKT/mTOR/FOXO3a Signaling Pathways." Nutrients 14, no. 9 (2022): 1859. http://dx.doi.org/10.3390/nu14091859.

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The present study aimed to investigate the effects of monotropein (MON) on improving dexamethasone (DEX)-induced muscle atrophy in mice and C2C12 mouse skeletal muscle cells. The body weights, grip strengths, and muscle weights of mice were assessed. The histological change in the gastrocnemius tissues was also observed through H&E staining. The expression of myosin heavy chain (MyHC), muscle ring finger 1 (MuRF1), and muscle atrophy F-box (Atrogin1) and the phosphorylation of AKT, mTOR, and FOXO3a in the muscle tissues of mice and C2C12 myotubes were analyzed using Western blotting. MON i

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Feng, Yongjia, Yu-Hwai Tsai, Weidong Xiao, et al. "Loss of ADAM17-Mediated Tumor Necrosis Factor Alpha Signaling in Intestinal Cells Attenuates Mucosal Atrophy in a Mouse Model of Parenteral Nutrition." Molecular and Cellular Biology 35, no. 21 (2015): 3604–21. http://dx.doi.org/10.1128/mcb.00143-15.

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Total parenteral nutrition (TPN) is commonly used clinically to sustain patients; however, TPN is associated with profound mucosal atrophy, which may adversely affect clinical outcomes. Using a mouse TPN model, removing enteral nutrition leads to decreased crypt proliferation, increased intestinal epithelial cell (IEC) apoptosis and increased mucosal tumor necrosis factor alpha (TNF-α) expression that ultimately produces mucosal atrophy. Upregulation of TNF-α signaling plays a central role in mediating TPN-induced mucosal atrophy without intact epidermal growth factor receptor (EGFR) signaling

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Berdeaux, Rebecca, and Randi Stewart. "cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism, and regeneration." American Journal of Physiology-Endocrinology and Metabolism 303, no. 1 (2012): E1—E17. http://dx.doi.org/10.1152/ajpendo.00555.2011.

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Among organ systems, skeletal muscle is perhaps the most structurally specialized. The remarkable subcellular architecture of this tissue allows it to empower movement with instructions from motor neurons. Despite this high degree of specialization, skeletal muscle also has intrinsic signaling mechanisms that allow adaptation to long-term changes in demand and regeneration after acute damage. The second messenger adenosine 3′,5′-monophosphate (cAMP) not only elicits acute changes within myofibers during exercise but also contributes to myofiber size and metabolic phenotype in the long term. St

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18

Li, Mengjie, Seong-Gook Kang, Kunlun Huang, and Tao Tong. "Streptococcus salivarius subsp. thermophilus ST-G30 Prevents Dexamethasone-Induced Muscle Atrophy in C2C12 Myotubes." Nutrients 17, no. 7 (2025): 1141. https://doi.org/10.3390/nu17071141.

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Background/Objectives: Sarcopenia is characterized by loss of muscle mass and strength and is associated with aging. Recently, its links with the gut–muscle axis have been reported, suggesting that probiotics could influence muscle health. Methods: In the present study, we investigated the protective roles of two lactic acid bacteria strains, Streptococcus salivarius subsp. thermophilus ST-G30 (ST-G30) and Lacticaseibacillus paracasei LPc-G110 (LPc-G110), on skeletal muscle atrophy induced by dexamethasone (DEX) in C2C12 myotubes. Results: Our results demonstrated that ST-G30 significantly all

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Batsukh, Sosorburam, Seyeon Oh, Kyoungmin Rheu, et al. "Rice Germ Attenuates Chronic Unpredictable Mild Stress-Induced Muscle Atrophy." Nutrients 15, no. 12 (2023): 2719. http://dx.doi.org/10.3390/nu15122719.

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Chronic stress leads to hypothalamic–pituitary–adrenal axis dysfunction, increasing cortisol levels. Glucocorticoids (GCs) promote muscle degradation and inhibit muscle synthesis, eventually causing muscle atrophy. In this study, we aimed to evaluate whether rice germ supplemented with 30% γ-aminobutyric acid (RG) attenuates muscle atrophy in an animal model of chronic unpredictable mild stress (CUMS). We observed that CUMS raised the adrenal gland weight and serum adrenocorticotropic hormone (ACTH) and cortisol levels, and these effects were reversed by RG. CUMS also enhanced the expression o

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Ramirez-Sanchez, Israel, Viridiana Navarrete, Leonor Galera, and Francisco Villarreal. "EFFECTS OF FLAVANOL (+)-EPICATECHIN ON SKELETAL MUSCLE OF AGED RATS." Innovation in Aging 6, Supplement_1 (2022): 801. http://dx.doi.org/10.1093/geroni/igac059.2890.

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Abstract Sarcopenia is a progressive and generalized age-related skeletal muscle (SkM) disorder characterized by the accelerated loss of muscle mass (atrophy) and function. SkM atrophy is associated with increased incidence of falls, functional decline, frailty and mortality. In its early stage, SkM atrophy is associated with oxidative stress, increased pro-inflammatory cytokine levels and proteasome-mediated protein degradation. These processes also link to the activation of atrophy associated factors and signaling pathways which lack any approved, targeted pharmacotherapy. We have characteri

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Schellekens, Willem-Jan M., Hieronymus W. H. van Hees, Michiel Vaneker, et al. "Toll-like Receptor 4 Signaling in Ventilator-induced Diaphragm Atrophy." Anesthesiology 117, no. 2 (2012): 329–38. http://dx.doi.org/10.1097/aln.0b013e3182608cc0.

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Background Mechanical ventilation induces diaphragm muscle atrophy, which plays a key role in difficult weaning from mechanical ventilation. The signaling pathways involved in ventilator-induced diaphragm atrophy are poorly understood. The current study investigated the role of Toll-like receptor 4 signaling in the development of ventilator-induced diaphragm atrophy. Methods Unventilated animals were selected for control: wild-type (n = 6) and Toll-like receptor 4 deficient mice (n = 6). Mechanical ventilation (8 h): wild-type (n = 8) and Toll-like receptor 4 deficient (n = 7) mice.Myosin heav

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Zaripova, Ksenia A., Svetlana P. Belova, Tatiana Y. Kostrominova, Boris S. Shenkman, and Tatiana L. Nemirovskaya. "Role of PI3 Kinases in Cell Signaling and Soleus Muscle Atrophy During Three Days of Unloading." International Journal of Molecular Sciences 26, no. 1 (2025): 414. https://doi.org/10.3390/ijms26010414.

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During skeletal muscle unloading, phosphoinositide 3-kinase (PI3K), and especially PI3K gamma (PI3Kγ), can be activated by changes in membrane potential. Activated IP3 can increase the ability of Ca2+ to enter the nucleus through IP3 receptors. This may contribute to the activation of transcription factors that initiate muscle atrophy processes. LY294002 inhibitor was used to study the role of PI3K in the ATP-dependent regulation of skeletal muscle signaling during three days of unloading. Inhibition of PI3K during soleus muscle unloading slows down the atrophic processes and prevents the accu

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Rodriguez, J., B. Vernus, I. Chelh, et al. "Myostatin and the skeletal muscle atrophy and hypertrophy signaling pathways." Cellular and Molecular Life Sciences 71, no. 22 (2014): 4361–71. http://dx.doi.org/10.1007/s00018-014-1689-x.

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Glass, David J. "A signaling role for dystrophin: Inhibiting skeletal muscle atrophy pathways." Cancer Cell 8, no. 5 (2005): 351–52. http://dx.doi.org/10.1016/j.ccr.2005.10.016.

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Liang, Jiling, Hu Zhang, Zhengzhong Zeng та ін. "Lifelong Aerobic Exercise Alleviates Sarcopenia by Activating Autophagy and Inhibiting Protein Degradation via the AMPK/PGC-1α Signaling Pathway". Metabolites 11, № 5 (2021): 323. http://dx.doi.org/10.3390/metabo11050323.

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Sarcopenia is an aging-induced syndrome characterized by a progressive reduction of skeletal muscle mass and strength. Increasing evidence has attested that appropriate and scientific exercise could induce autophagy or optimize the functional status of autophagy, which plays a critical role in senescent muscular dystrophy. As a publicly recognized strategy for extending lifespan and improving the health of the elderly, the underlying mechanisms of lifelong regular aerobic exercise for the prevention of sarcopenia have not been fully elucidated. To explore the role of lifelong aerobic exercise

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Yadav, Aarti, Anil Dahuja, and Rajesh Dabur. "Dynamics of Toll-like Receptors Signaling in Skeletal Muscle Atrophy." Current Medicinal Chemistry 28, no. 28 (2021): 5831–46. http://dx.doi.org/10.2174/0929867328666210202113734.

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Skeletal muscle atrophy has been characterized as a state of uncontrolled inflammation and oxidative stress that escalates protein catabolism. Recent advancement supports impinging signaling molecules in the muscle fibers controlled through toll-like receptors (TLR). Activated TLR signaling pathways have been identified as inhibitors of muscle mass and provoke the settings for muscle atrophy. Among them, mainly TLR2 and TLR4 manifest their presence to exacerbate the release of the pro-inflammatory cytokine to deform the synchronized muscle programming. The present review enlightens the TLR sig

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Sun, Chen-Chen, Zuo-Qiong Zhou, Zhang-Lin Chen, et al. "Identification of Potentially Related Genes and Mechanisms Involved in Skeletal Muscle Atrophy Induced by Excessive Exercise in Zebrafish." Biology 10, no. 8 (2021): 761. http://dx.doi.org/10.3390/biology10080761.

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Long-term imbalance between fatigue and recovery may eventually lead to muscle weakness or even atrophy. We previously reported that excessive exercise induces pathological cardiac hypertrophy. However, the effect of excessive exercise on the skeletal muscles remains unclear. In the present study, we successfully established an excessive-exercise-induced skeletal muscle atrophy zebrafish model, with decreased muscle fiber size, critical swimming speed, and maximal oxygen consumption. High-throughput RNA-seq analysis identified differentially expressed genes in the model system compared with co

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Mañas-García, Laura, Nuria Bargalló, Joaquim Gea, and Esther Barreiro. "Muscle Phenotype, Proteolysis, and Atrophy Signaling During Reloading in Mice: Effects of Curcumin on the Gastrocnemius." Nutrients 12, no. 2 (2020): 388. http://dx.doi.org/10.3390/nu12020388.

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We hypothesized that curcumin may mitigate muscle protein degradation and loss through attenuation of proteolytic activity in limb muscles of mice exposed to reloading (7dR) following immobilization (7dI). In gastrocnemius of mice (female C57BL/6J, 10 weeks) exposed to recovery following a seven-day period of hindlimb immobilization with/without curcumin treatment, markers of muscle proteolysis (systemic troponin-I), atrophy signaling pathways and histone deacetylases, protein synthesis, and muscle phenotypic characteristics and function were analyzed. In gastrocnemius of reloading mice compar

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Lee, Eun-Joo, and Ronald L. Neppl. "Influence of Age on Skeletal Muscle Hypertrophy and Atrophy Signaling: Established Paradigms and Unexpected Links." Genes 12, no. 5 (2021): 688. http://dx.doi.org/10.3390/genes12050688.

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Skeletal muscle atrophy in an inevitable occurrence with advancing age, and a consequence of disease including cancer. Muscle atrophy in the elderly is managed by a regimen of resistance exercise and increased protein intake. Understanding the signaling that regulates muscle mass may identify potential therapeutic targets for the prevention and reversal of muscle atrophy in metabolic and neuromuscular diseases. This review covers the major anabolic and catabolic pathways that regulate skeletal muscle mass, with a focus on recent progress and potential new players.

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Cheng, Jingfei, Wei Zhou, Gina M. Warner, et al. "Temporal analysis of signaling pathways activated in a murine model of two-kidney, one-clip hypertension." American Journal of Physiology-Renal Physiology 297, no. 4 (2009): F1055—F1068. http://dx.doi.org/10.1152/ajprenal.90439.2008.

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Unilateral renal artery stenosis (RAS) leads to atrophy of the stenotic kidney and compensatory enlargement of the contralateral kidney. Although the two-kidney, one-clip (2K1C) model has been extensively used to model human RAS, the cellular responses in the stenotic and contralateral kidneys, particularly in the murine model, have received relatively little attention. We studied mice 2, 5, and 11 wk after unilateral RAS. These mice became hypertensive within 1 wk. The contralateral kidney increased in size within 2 wk after surgery. This enlargement was associated with a transient increase i

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Costa, Alessandra, Angelica Toschi, Ivana Murfuni, et al. "Local Overexpression of V1a-Vasopressin Receptor Enhances Regeneration in Tumor Necrosis Factor-Induced Muscle Atrophy." BioMed Research International 2014 (2014): 1–14. http://dx.doi.org/10.1155/2014/235426.

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Skeletal muscle atrophy occurs during disuse and aging, or as a consequence of chronic diseases such as cancer and diabetes. It is characterized by progressive loss of muscle tissue due to hypotrophic changes, degeneration, and an inability of the regeneration machinery to replace damaged myofibers. Tumor necrosis factor (TNF) is a proinflammatory cytokine known to mediate muscle atrophy in many chronic diseases and to inhibit skeletal muscle regeneration. In this study, we investigated the role of Arg-vasopressin-(AVP-)dependent pathways in muscles in which atrophy was induced by local overex

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Mahmassani, Ziad S., Paul T. Reidy, Alec I. McKenzie, Chris Stubben, Michael T. Howard, and Micah J. Drummond. "Age-dependent skeletal muscle transcriptome response to bed rest-induced atrophy." Journal of Applied Physiology 126, no. 4 (2019): 894–902. http://dx.doi.org/10.1152/japplphysiol.00811.2018.

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Short-term muscle disuse induces significant muscle loss in older adults and in some reports may be more accelerated with aging. Identifying muscle transcriptional events in response to bed rest may help identify therapeutic targets to offset muscle loss. Therefore, we compared the muscle transcriptome between young and older adults after bed rest and identified candidate targets related to changes in muscle loss. RNA was sequenced (HiSeq, Illumina; DESeq, R) from muscle biopsies obtained from young [ n = 9; 23 yr (SD 3)] and older [ n = 18; 68 yr (SD 6)] adults before and after 5-day bed rest

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Fox, Daniel K., Scott M. Ebert, Kale S. Bongers, et al. "p53 and ATF4 mediate distinct and additive pathways to skeletal muscle atrophy during limb immobilization." American Journal of Physiology-Endocrinology and Metabolism 307, no. 3 (2014): E245—E261. http://dx.doi.org/10.1152/ajpendo.00010.2014.

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Immobilization causes skeletal muscle atrophy via complex signaling pathways that are not well understood. To better understand these pathways, we investigated the roles of p53 and ATF4, two transcription factors that mediate adaptations to a variety of cellular stresses. Using mouse models, we demonstrate that 3 days of muscle immobilization induces muscle atrophy and increases expression of p53 and ATF4. Furthermore, muscle fibers lacking p53 or ATF4 are partially resistant to immobilization-induced muscle atrophy, and forced expression of p53 or ATF4 induces muscle fiber atrophy in the abse

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Russell, Sarah J., and Martin F. Schneider. "Alternative signaling pathways from IGF1 or insulin to AKT activation and FOXO1 nuclear efflux in adult skeletal muscle fibers." Journal of Biological Chemistry 295, no. 45 (2020): 15292–306. http://dx.doi.org/10.1074/jbc.ra120.013634.

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Muscle atrophy is regulated by the balance between protein degradation and synthesis. FOXO1, a transcription factor, helps to determine this balance by activating pro-atrophic gene transcription when present in muscle fiber nuclei. Foxo1 nuclear efflux is promoted by AKT-mediated Foxo1 phosphorylation, eliminating FOXO1's atrophy-promoting effect. AKT activation can be promoted by insulin-like growth factor 1 (IGF1) or insulin via a pathway including IGF1 or insulin, phosphatidylinositol 3-kinase, and AKT. We used confocal fluorescence time-lapse imaging of FOXO1–GFP in adult isolated living m

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Hsu, Te-Hsing, Ting-Jian Wu, Yu-An Tai, Chin-Shiu Huang, Jiunn-Wang Liao, and Shu-Lan Yeh. "The combination of quercetin and leucine synergistically improves grip strength by attenuating muscle atrophy by multiple mechanisms in mice exposed to cisplatin." PLOS ONE 18, no. 9 (2023): e0291462. http://dx.doi.org/10.1371/journal.pone.0291462.

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Both quercetin and leucine have been shown to exert moderately beneficial effects in preventing muscle atrophy induced by cancers or chemotherapy. However, the combined effects of quercetin and leucine, as well as the possible underlying mechanisms against cisplatin (CDDP)-induced muscle atrophy and cancer-related fatigue (CRF) remain unclear. To investigate the issues, male BALB/c mice were randomly assigned to the following groups for 9 weeks: Control, CDDP (3 mg/kg/week), CDDP+Q (quercetin 200 mg/kg/day administrated by gavage), CDDP+LL (a diet containing 0.8% leucine), CDDP+Q+LL, CDDP+HL (

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Feng, Yongjia, та Daniel H. Teitelbaum. "Epidermal growth factor/TNF-α transactivation modulates epithelial cell proliferation and apoptosis in a mouse model of parenteral nutrition". American Journal of Physiology-Gastrointestinal and Liver Physiology 302, № 2 (2012): G236—G249. http://dx.doi.org/10.1152/ajpgi.00142.2011.

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Epidermal growth factor (EGF) and tumor necrosis factor-α (TNF-α) signaling are critical for effective proliferative and apoptotic actions; however, little is known about the codependency of these signaling pathways in the intestinal epithelium. Because total parenteral nutrition (TPN) is associated with loss of intestinal epithelial cell (IEC) proliferation and increased apoptosis, we utilized a mouse model to explore these transactivation pathways in small bowel epithelium. Mice underwent intravenous cannulation and were given enteral nutrition or TPN for 7 days. Outcomes included IEC prolif

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Woodland, Robert T., Casey J. Fox, Madelyn R. Schmidt, et al. "Multiple signaling pathways promote B lymphocyte stimulator–dependent B-cell growth and survival." Blood 111, no. 2 (2008): 750–60. http://dx.doi.org/10.1182/blood-2007-03-077222.

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We investigated the mechanism by which B lymphocyte stimulator (BLyS)/BAFF, a tumor necrosis factor superfamily ligand, promotes B-cell survival and resistance to atrophy. BLyS stimulation activates 2 independent signaling pathways, Akt/mTOR and Pim 2, associated with cell growth and survival. BLyS blocks the cell volume loss (atrophy) that freshly isolated B cells normally undergo when maintained in vitro while concurrently increasing glycolytic activity and overall metabolism. This atrophy resistance requires Akt/mTOR. We used a genetic approach to resolve the contributions of Akt/mTOR and P

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Lee, Hee-Jeong, Dongwook Kim, Yousung Jung, Soomin Oh, Cho Hee Kim, and Aera Jang. "Horse Meat Hydrolysate Ameliorates Dexamethasone-Induced Muscle Atrophy in C57BL/6 Mice via the AKT/FoxO3a/mTOR Pathway." Cells 14, no. 14 (2025): 1050. https://doi.org/10.3390/cells14141050.

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As life expectancy increases, muscle atrophy, characterized by a decline in muscle mass and strength that can impair mobility, has become a growing concern, highlighting the potential of protein supplementation as a promising intervention strategy. A horse meat hydrolysate, with a molecular weight of less than 3 kDa, derived from m. biceps femoris and produced using the food-grade enzyme Alcalase® (A4 < 3kDa) was evaluated for its efficacy in mitigating dexamethasone-induced muscle atrophy, a widely accepted model for studying catabolic muscle loss. Administered orally to C57BL/6 mice at do

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Weng, Shaoting, Feng Gao, Juan Wang, et al. "Improvement of muscular atrophy by AAV–SaCas9-mediated myostatin gene editing in aged mice." Cancer Gene Therapy 27, no. 12 (2020): 960–75. http://dx.doi.org/10.1038/s41417-020-0178-7.

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AbstractMuscle mass and area usually decrease with age, and this phenomenon is known as sarcopenia. This age-related atrophy correlates with insufficient levels of muscle cells differentiate and proliferate regulated by the TGF-β signaling pathway and the expression of E3s ubiquitin-protein ligase by the aged. Sarcopenia makes a huge impact on the aging society, because it has the characteristic of high incidence, extensive adverse effects and disease aggravation gradually. Guided by a single-guide RNA (sgRNA), Cas9 nuclease has been widely used in genome editing, opening up a new pathway for

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Childs, Thomas E., Espen E. Spangenburg, Dharmesh R. Vyas, and Frank W. Booth. "Temporal alterations in protein signaling cascades during recovery from muscle atrophy." American Journal of Physiology-Cell Physiology 285, no. 2 (2003): C391—C398. http://dx.doi.org/10.1152/ajpcell.00478.2002.

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Currently, the repertoire of cellular and molecular pathways that control skeletal muscle atrophy and hypertrophy are not well defined. It is possible that intracellular regulatory signaling pathways are active at different times during the muscle hypertrophy process. The hypothesis of the given experiments was that cellular signals related to protein translation would be active at early time points of skeletal muscle regrowth, whereas transcriptional signals would be active at later time points of skeletal muscle regrowth. The phosphorylation status of p38 MAPK and JNK increased at the end of

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Hensel, Niko, Federica Cieri, Pamela Santonicola, et al. "Impairment of the neurotrophic signaling hub B-Raf contributes to motoneuron degeneration in spinal muscular atrophy." Proceedings of the National Academy of Sciences 118, no. 18 (2021): e2007785118. http://dx.doi.org/10.1073/pnas.2007785118.

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Spinal muscular atrophy (SMA) is a motoneuron disease caused by deletions of the Survival of Motoneuron 1 gene (SMN1) and low SMN protein levels. SMN restoration is the concept behind a number of recently approved drugs which result in impressive yet limited effects. Since SMN has already been enhanced in treated patients, complementary SMN-independent approaches are needed. Previously, a number of altered signaling pathways which regulate motoneuron degeneration have been identified as candidate targets. However, signaling pathways form networks, and their connectivity is still unknown in SMA

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Rajasekaran, M. Raj, Sadhana Kanoo, Johnny Fu, My-Uyen (Lilly) Nguyen, Valmik Bhargava та Ravinder K. Mittal. "Age-related external anal sphincter muscle dysfunction and fibrosis: possible role of Wnt/β-catenin signaling pathways". American Journal of Physiology-Gastrointestinal and Liver Physiology 313, № 6 (2017): G581—G588. http://dx.doi.org/10.1152/ajpgi.00209.2017.

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Studies show an age-related increase in the prevalence of anal incontinence and sphincter muscle atrophy. The Wnt/β-catenin signaling pathway has been recently recognized as the major molecular pathway involved in age-related skeletal muscle atrophy and fibrosis. The goals of our study were to 1) evaluate the impact of normal aging on external anal sphincter (EAS) muscle length-tension (L-T) function and morphology and 2) specifically examine the role of Wnt signaling pathways in anal sphincter muscle fibrosis. New Zealand White female rabbits [6 young (6 mo of age) and 6 old (36 mo of age)] w

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Li, Wenan, Kaishu Deng, Mengyue Zhang, et al. "Network Pharmacology Combined with Experimental Validation to Investigate the Effects and Mechanisms of Aucubin on Aging-Related Muscle Atrophy." International Journal of Molecular Sciences 26, no. 6 (2025): 2626. https://doi.org/10.3390/ijms26062626.

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Aucubin (AU) is one of the main components of the traditional Chinese medicine Eucommia ulmoides Oliv (EU). This study investigated the effects of AU on aging-related skeletal muscle atrophy in vitro and in vivo. The results of network pharmacology revealed the potential therapeutic effects of AU on muscle atrophy. In vitro, AU effectively attenuated D-gal-induced cellular damage, reduced the number of senescence-associated β-galactosidase (SA-β-Gal)-positive cells, down-regulated the expression levels of muscle atrophy-related proteins Atrogin-1 and MuRF1, and improved myotube differentiation

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Lee, Min-Kyeong, Jeong-Wook Choi, Youn Choi, and Taek-Jeong Nam. "Pyropia yezoensis Protein Supplementation Prevents Dexamethasone-Induced Muscle Atrophy in C57BL/6 Mice." Marine Drugs 16, no. 9 (2018): 328. http://dx.doi.org/10.3390/md16090328.

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We investigated the protective effects of Pyropia yezoensis crude protein (PYCP) against dexamethasone (DEX)-induced myotube atrophy and its underlying mechanisms. DEX (3 mg/kg body weight, intraperitoneal injection) and PYCP (150 and 300 mg/kg body weight, oral) were administrated to mice for 18 days, and the effects of PYCP on DEX-induced muscle atrophy were evaluated. Body weight, calf thickness, and gastrocnemius and tibialis anterior muscle weight were significantly decreased by DEX administration (p < 0.05), while PYCP supplementation effectively prevented the DEX-induced decrease in

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Biondi, O., J. Branchu, A. Ben Salah, et al. "IGF-1R Reduction Triggers Neuroprotective Signaling Pathways in Spinal Muscular Atrophy Mice." Journal of Neuroscience 35, no. 34 (2015): 12063–79. http://dx.doi.org/10.1523/jneurosci.0608-15.2015.

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Jit, Bimal Prasad, Biswajita Pradhan, Rutumbara Dash, et al. "Phytochemicals: Potential Therapeutic Modulators of Radiation Induced Signaling Pathways." Antioxidants 11, no. 1 (2021): 49. http://dx.doi.org/10.3390/antiox11010049.

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Ionizing radiation results in extensive damage to biological systems. The massive amount of ionizing radiation from nuclear accidents, radiation therapy (RT), space exploration, and the nuclear battlefield leads to damage to biological systems. Radiation injuries, such as inflammation, fibrosis, and atrophy, are characterized by genomic instability, apoptosis, necrosis, and oncogenic transformation, mediated by the activation or inhibition of specific signaling pathways. Exposure of tumors or normal cells to different doses of ionizing radiation could lead to the generation of free radical spe

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Ito, Naoki, Urs Ruegg, and Shin’ichi Takeda. "ATP-Induced Increase in Intracellular Calcium Levels and Subsequent Activation of mTOR as Regulators of Skeletal Muscle Hypertrophy." International Journal of Molecular Sciences 19, no. 9 (2018): 2804. http://dx.doi.org/10.3390/ijms19092804.

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Intracellular signaling pathways, including the mammalian target of rapamycin (mTOR) and the mitogen-activated protein kinase (MAPK) pathway, are activated by exercise, and promote skeletal muscle hypertrophy. However, the mechanisms by which these pathways are activated by physiological stimulation are not fully understood. Here we show that extracellular ATP activates these pathways by increasing intracellular Ca2+ levels ([Ca2+]i), and promotes muscle hypertrophy. [Ca2+]i in skeletal muscle was transiently increased after exercise. Treatment with ATP induced the increase in [Ca2+]i through

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Zaripova, К. А., S. P. Belova, B. S. Shenkman, and Т. L. Nemirovskaya. "INHIBITION OF THE PI3KS SLOWS DOWN ATROPHY DEVELOPMENT IN RAT'S M. SOLEUS AFTER 3-DAY FUNCTIONAL DISLOADING." Aerospace and Environmental Medicine 58, no. 6 (2024): 68–75. https://doi.org/10.21687/0233-528x-2024-58-6-68-75.

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Phosphoinositide-3-kinase (PI3K) (PI3Kγ, specifically) can be activated by a change in the membrane potential due to muscle functional unloading; as a result, IP3 enhances Ca2+ entry in the nucleus via IS3R. This benefits activation of the transcriptional factors that trigger atrophy. Inhibitor LY294002 was used to explore the PI3K role in ATP-dependent regulation of signaling in rat's muscles after 3-day suspension. PI3K inhibition after functional unloading slows down m. soleus atrophy, prevents ATP deposition, and expression of Е3-ubuquitine ligase MuRF1 and ubuquitine, prevents rise in exp

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Jiang, Lingong, Huimin Jia, Zhicheng Tang, et al. "Proteomic Analysis of Radiation-Induced Acute Liver Damage in a Rabbit Model." Dose-Response 17, no. 4 (2019): 155932581988950. http://dx.doi.org/10.1177/1559325819889508.

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Radiation-induced liver damage (RILD) has become a limitation in radiotherapy for hepatocellular carcinoma. We established a rabbit model of RILD by CyberKnife. Electron microscopy analysis revealed obvious nuclear atrophy and disposition of fat in the nucleus after irradiation. We then utilized a mass spectrometry-based label-free relative quantitative proteomics approach to compare global proteomic changes of rabbit liver in response to radiation. In total, 2365 proteins were identified, including 338 proteins that were significantly dysregulated between irradiated and nonirradiated liver ti

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Peris-Moreno, Dulce, Laura Cussonneau, Lydie Combaret, Cécile Polge, and Daniel Taillandier. "Ubiquitin Ligases at the Heart of Skeletal Muscle Atrophy Control." Molecules 26, no. 2 (2021): 407. http://dx.doi.org/10.3390/molecules26020407.

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Skeletal muscle loss is a detrimental side-effect of numerous chronic diseases that dramatically increases mortality and morbidity. The alteration of protein homeostasis is generally due to increased protein breakdown while, protein synthesis may also be down-regulated. The ubiquitin proteasome system (UPS) is a master regulator of skeletal muscle that impacts muscle contractile properties and metabolism through multiple levers like signaling pathways, contractile apparatus degradation, etc. Among the different actors of the UPS, the E3 ubiquitin ligases specifically target key proteins for ei

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