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The Role of Exercise in Cancer-Related Sarcopenia and Sarcopenic Obesity.

One of the most common adverse effects of cancer and its therapeutic strategies is sarcopenia, a condition which is characterised by excess muscle wasting and muscle strength loss due to the disrupted muscle homeostasis. Moreover, cancer-related sarcopenia may be combined with the increased deposition of fat mass, a syndrome called cancer-associated sarcopenic obesity. Both clinical conditions have significant clinical importance and can predict disease progression and survival. A growing body of evidence supports the claim that physical exercise is a safe and effective complementary therapy f

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… Nevertheless, the most widely studied myokine for its role in sarcopenia is myostatin (Mstn). Myostatin expression is muscle-specific and leads to protein breakdown and atrophy via binding to activin receptor type-IIB (ActRIIB), a TGF-β superfamily receptor [ 157 , 158 ]. … ActA retains similar actions with myostatin, since it utilises the ActRIIB receptor, and thus regulates the cancer-related muscle atrophy and cachexia [ 168 ]. …

Cancer cachexia--pathophysiology and management.

About half of all cancer patients show a syndrome of cachexia, characterized by anorexia and loss of adipose tissue and skeletal muscle mass. Cachexia can have a profound impact on quality of life, symptom burden, and a patient's sense of dignity. It is a very serious complication, as weight loss during cancer treatment is associated with more chemotherapy-related side effects, fewer completed cycles of chemotherapy, and decreased survival rates. Numerous cytokines have been postulated to play a role in the etiology of cancer cachexia. Cytokines can elicit effects that mimic leptin signaling a

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… Myostatin Myostatin is an extracellular cytokine that is mostly expressed in skeletal muscles and is known to play a crucial role in the negative regulation of muscle mass [ 56 ]. … Akt is the ‘crossing point’ between the IGF-1 and myostatin pathways [ 56 ]. …

Abstracts of the 5(th) Cachexia Conference, Barcelona, Spain, December 5-8, 2009.

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… Concurrently, MAFbx ( P < 0.001), MuRF1 ( P < 0.001), 20S proteasome ( P < 0.001), cathepsin- l ( P < 0.01), and myostatin ( P < 0.05) mRNA increased in CIP and was matched by an increase in MAFbx ( P < 0.05), MuRF1 ( P < 0.05), 20S proteasome ( P < 0.05), and myostatin ( P < 0.001) protein expression … Additionally, CIP presented with increased MAFbx, MuRF1, 20S proteasome, and myostatin mRNA expression, which was paralleled by increased expression at the protein level. 009 Muscle wasting in patients with chronic obstructive pulmonary disease (COPD) Hegoi Segurola, Cleofé Pérez-Portabella, Jaume …

Development of a reliable automated screening system to identify small molecules and biologics that promote human β-cell regeneration.

Numerous compounds stimulate rodent β-cell proliferation; however, translating these findings to human β-cells remains a challenge. To examine human β-cell proliferation in response to such compounds, we developed a medium-throughput in vitro method of quantifying adult human β-cell proliferation markers. This method is based on high-content imaging of dispersed islet cells seeded in 384-well plates and automated cell counting that identifies fluorescently labeled β-cells with high specificity using both nuclear and cytoplasmic markers. β-Cells from each donor were assessed for their function

Chemotherapy-related cachexia is associated with mitochondrial depletion and the activation of ERK1/2 and p38 MAPKs.

Cachexia affects the majority of cancer patients, with currently no effective treatments. Cachexia is defined by increased fatigue and loss of muscle function resulting from muscle and fat depletion. Previous studies suggest that chemotherapy may contribute to cachexia, although the causes responsible for this association are not clear. The purpose of this study was to investigate the mechanism(s) associated with chemotherapy-related effects on body composition and muscle function. Normal mice were administered chemotherapy regimens used for the treatment of colorectal cancer, such as Folfox (

Muscle wasting in cancer: opportunities and challenges for exercise in clinical cancer trials.

BACKGROUND: Low muscle in cancer is associated with an increase in treatment-related toxicities and is a predictor of cancer-related and all-cause mortality. The mechanisms of cancer-related muscle loss are multifactorial, including anorexia, hypogonadism, anaemia, inflammation, malnutrition, and aberrations in skeletal muscle protein turnover and metabolism. METHODS: In this narrative review, we summarise relevant literature to (i) review the factors influencing skeletal muscle mass regulation, (ii) provide an overview of how cancer/treatments negatively impact these, (iii) review factors be

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… of genes involved in muscle homeostasis. 45 Additionally, myostatin activates AMPK during energy stress to increase nutrient availability. 47 Collectively, myostatin’s ability to interact with these other important regulatory and signalling proteins demonstrates its significant roles in the multiple … The role of myostatin in muscle wasting: an overview . J Cachexia Sarcopenia Muscle 2011 ; 2 : 143 – 151 . 21966641 10.1007/s13539-011-0035-5 PMC3177043 46. Lee SJ . Regulation of muscle mass by myostatin . …

Safety and efficacy of apitegromab in nonambulatory type 2 or type 3 spinal muscular atrophy (SAPPHIRE): a phase 3, double-blind, randomised, placebo-controlled trial.

BACKGROUND: Approved spinal muscular atrophy therapies greatly improve clinical outcomes; however, substantial motor function deficits persist. Apitegromab, a fully human monoclonal antibody, selectively inhibits myostatin activation, improving muscle function. We aimed to assess the safety and efficacy of apitegromab in patients with nonambulatory type 2 or type 3 spinal muscular atrophy receiving nusinersen or risdiplam. METHODS: SAPPHIRE, a double-blind, placebo-controlled, phase 3 trial, was done in 48 hospitals in Belgium, France, Germany, Italy, Poland, Spain, the Netherlands, the UK, a…

The Role of Extracellular Vesicles (EVs) in the Epigenetic Regulation of Bone Metabolism and Osteoporosis.

Extracellular vesicles (EVs) are complex phospholipidic structures actively released by cells. EVs are recognized as powerful means of intercellular communication since they contain many signaling molecules (including lipids, proteins, and nucleic acids). In parallel, changes in epigenetic processes can lead to changes in gene function and finally lead to disease onset and progression. Recent breakthroughs have revealed the complex roles of non-coding RNAs (microRNAs (miRNAs) and long non-coding RNAs (lncRNAs)) in epigenetic regulation. Moreover, a substantial body of evidence demonstrates tha

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… Moreover, muscle secretes a set of molecules, known as myokines, directly affecting bone metabolism, such as irisin, myostatin, and insulin-like growth factor-1 [ 29 ]. 1.2. … Serum levels of muscle-derived cytokine myostatin increase with progressing age both in men and in women and are inversely associated with skeletal muscle mass [ 145 , 146 ]. Qin et al. showed that high levels of myostatin affect bone cells, especially osteocytes. …

Protein breakdown in muscle wasting: role of autophagy-lysosome and ubiquitin-proteasome.

Skeletal muscle adapts its mass as consequence of physical activity, metabolism and hormones. Catabolic conditions or inactivity induce signaling pathways that regulate the process of muscle loss. Muscle atrophy in adult tissue occurs when protein degradation rates exceed protein synthesis. Two major protein degradation pathways, the ubiquitin-proteasome and the autophagy-lysosome systems, are activated during muscle atrophy and variably contribute to the loss of muscle mass. These degradation systems are controlled by a transcription dependent program that modulates the expression of rate-lim

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… PGC-1α4 was found to induce IGF1 and repress myostatin, thus promoting hypertrophy and reducing muscle atrophy during cancer or hindlimb suspension. … Interestingly, also JunB markedly suppresses myostatin expression in transfected myotubes and decreases the phosphorylation of Smad3, the transcription factor downstream of the myostatin-TGFβ signaling pathway ( Raffaello et al., 2010 ). …

Potential Adverse Effects of Dexamethasone Therapy on COVID-19 Patients: Review and Recommendations.

In the context of the coronavirus disease 2019 (COVID-19) pandemic, the global healthcare community has raced to find effective therapeutic agents against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). To date, dexamethasone is the first and an important therapeutic to significantly reduce the risk of death in COVID-19 patients with severe disease. Due to powerful anti-inflammatory and immunosuppressive effects, dexamethasone could attenuate SARS-CoV-2-induced uncontrolled cytokine storm, severe acute respiratory distress syndrome and lung injury. Nevertheless, dexamethasone tre

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… Qin et al. observed that the upregulation of myostatin gene expression caused by dexamethasone was associated with the myostatin gene promoter and glucocorticoid responsive element along the promoter [ 73 ], and the increased myostatin led to the changes in ultrastructure of skeletal muscle, including … Zimmers TA Davies MV Koniaris LG Induction of cachexia in mice by systemically administered myostatin Science 2002 296 1486 1488 12029139 10.1126/science.1069525 76. …

Development and Differentiation in Monobodies Based on the Fibronectin Type 3 Domain.

As a non-antibody scaffold, monobodies based on the fibronectin type III (FN3) domain overcome antibody size and complexity while maintaining analogous binding loops. However, antibodies and their derivatives remain the gold standard for the design of new therapeutics. In response, clinical-stage therapeutic proteins based on the FN3 domain are beginning to use native fibronectin function as a point of differentiation. The small and simple structure of monomeric monobodies confers increased tissue distribution and reduced half-life, whilst the absence of disulphide bonds improves stability in

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… Fibronectin-based scaffold domain proteins that bind myostatin: A patent evaluation of WO2014043344. Expert Opin. Ther. Pat. 2015;25:619–624. doi: 10.1517/13543776.2015.1007954. 76. … BMS-986089: A novel adnectin protein that dose dependently lowers free myostatin and increases muscle volume and lean body mass. Neuromuscul. Disord. 2016;26:S95. doi: 10.1016/j.nmd.2016.06.037. 90. …

Activin Receptor-Ligand Trap for the Treatment of β-thalassemia: A Serendipitous Discovery.

β-thalassemia is a hereditary disorder caused by defective production of β-globin chains of hemoglobin (Hb) that leads to an increased α/β globins ratio with subsequent free α-globins. Alpha globin excess causes oxidative stress, red blood cells membrane damage, premature death of late-stage erythroid precursors, resulting in ineffective erythropoiesis. The transforming growth factor β (TGF-β) superfamily signaling acts on biological processes, such as cell quiescence, apoptosis, proliferation, differentiation, and migration, and plays an essential role in regulating the hematopoiesis. This pa

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… The myostatin propeptide and the follistatin-related gene are inhibitory binding proteins of myostatin in normal serum. J Biol Chem. 2002;277(43):40735–41. doi: 10.1074/jbc.M206379200. 14. Lewis KA, Gray PC, Blount AL, MacConell LA, Wiater E, Bilezikjian LM, et al. … Expression of myostatin in human hematopoietic cells unveils novel autocrine/paracrine actions for the hormone. J Cell Physiol. 2019;234(5):7236–46. doi: 10.1002/jcp.27494. 20. Rochette L, Zeller M, Cottin Y, Vergely C. …

Role of growth differentiation factor 15 in cancer cachexia (Review).

Growth differentiation factor 15 (GDF15), a member of the transforming growth factor-β family, is a stress-induced cytokine. Under normal circumstances, the expression of GDF15 is low in most tissues. It is highly expressed during tissue injury, inflammation, oxidative stress and cancer. GDF15 has been established as a biomarker in patients with cancer, and is associated with cancer cachexia (CC) and poor survival. CC is a multifactorial metabolic disorder characterized by severe muscle and adipose tissue atrophy, loss of appetite, anemia and bone loss. Cachexia leads to reductions in quality

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… Systemic inflammation is characterized by increased circulating levels of cytokines, including tumor necrosis factor (TNF)-α, TNF-like weak inducer of apoptosis, interleukin (IL)-1, IL-6, IL-8, IL-20, interferon-γ, leukemia inhibitory factor, myostatin, activin and growth differentiation factor 15 (GDF15 … , activin, TNF-α | ( 10 , 18 – 21 ) Gallbladder | Cholestasis | IL-6 | ( 19 ) Bone | Osteoclast activation, bone loss, hypercalcemia | IL-6 | ( 6 , 22 ) Pancreas | Insulin resistance | TNF-α | ( 13 , 21 ) Spleen | Splenomegaly | Myostatin, activin | ( 18 ) Intestine | Intestinal barrier dysfunction, …

Elevated serum Activin A in chronic obstructive pulmonary disease with skeletal muscle wasting.

OBJECTIVE: Muscle wasting contributes to the reduced quality of life and increased mortality in chronic obstructive pulmonary disease (COPD). Muscle atrophy in mice with cachexia was caused by Activin A binding to ActRIIB. The role of circulating Activin A leading to muscle atrophy in COPD remains elusive. METHODS: In the present study, we evaluated the relationship between serum levels of Activin A and skeletal muscle wasting in COPD patients. The expression levels of serum Activin A were measured in 78 stable COPD patients and in 60 healthy controls via ELISA, which was also used to determi

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… In addition to abnormal conditions, such as denervation, fasting, disuse, oxidative stress and hypoxia 25-27 , a number of factors, such as myostatin and Act A, are responsible for muscle weakness due to protein degradation and intrinsic metabolic abnormalities 28 , 29 . … manner via keratinocytes Am J Pathol 2005 167 3 733 47 10.1016/S0002-9440(10)62047-0 16127153 PMC1698729 32 Clotman F Lemaigre FP Control of hepatic differentiation by activin/TGFbeta signaling Cell Cycle 2006 5 2 168 71 10.4161/cc.5.2.2341 16357531 33 Thissen JP Loumaye A [Role of Activin A and Myostatin …

Potential of Lycii Radicis Cortex as an Ameliorative Agent for Skeletal Muscle Atrophy.

Lycii Radicis Cortex (LRC) is a traditional medicine in East Asia with various beneficial effects, including antioxidant, anti-inflammatory, anti-tumor, anti-diabetic, and anti-depressant properties. However, its potential effects on skeletal muscle atrophy have not been studied. In this study, the protective effects of LRC extract (LRCE) on dexamethasone (DEX)-induced muscle atrophy were investigated in C2C12 myotubes and mice. We evaluated the effect of LRCE on improving muscle atrophy using a variety of methods, including immunofluorescence staining, quantitative polymerase chain reaction (

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… Furthermore, co-treatment of C2C12 myotubes with LRCE (50 and 100 µg/mL) and DEX resulted in lower mRNA levels of myostatin, MuRF1, and atrogin-1 compared to DEX-treated myotubes ( Figure 2 A). … In this study, compared to the DEX group, treatment with LCRE resulted in the upregulation of myogenin mRNA levels and MHC protein, while myostatin, murf1, and atrogin-1 mRNA levels, as well as MuRF1 protein, were downregulated ( Figure 2 ). …

Impact of whole-body vibration exercise on physical performance and bone turnover in patients with monoclonal gammopathy of undetermined significance.

OBJECTIVE: Monoclonal Gammopathy of Undetermined Significance (MGUS) is a risk factor for reduced physical performance, osteoporosis, and fractures due to compromised musculoskeletal metabolism. In this condition it is unknown whether whole-body vibration (WBV) exercise favorably alters physical performance and bone metabolism. METHODS: To evaluate the effect of three-months WBV exercise (30 min; 2x/week) including an optional three-month extension on physical performance, bone metabolism and bone mineral density. Endpoints included functional assessments, bone turnover markers and bone miner

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… DKK-1, sclerostin, bone-specific alkaline phosphatase, and myostatin were assessed by an external supplier (Immundiagnostik AG, Bensheim, Germany). … Myostatin levels did not change over the course of the study (p = 0.865; p = 0.445 at three and six months). Further markers including calcium, creatinine, hemoglobin and M−protein levels revealed only minor changes over time with no consistent trend ( Table 4 ). …

Recent Articles-Skeletal Muscle and Other Topics in Diabetes.

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… Recent efforts have targeted the myostatin pathway, which physiologically leads to inhibition of muscle growth [ 11 ]. Bimagrumab, an activin receptor antagonist, promotes skeletal muscle growth and fat loss, and may have benefits for bone health. … W., “Myostatin/Activin Receptor Ligands in Muscle and the Development Status of Attenuating Drugs,” Endocrine Reviews 43, no. 2 (March 2022): 329–365. 12. Garito T., Zakaria M., Papanicolaou D. …

Gene and protein expression associated with protein synthesis and breakdown in paraplegic skeletal muscle.

Spinal cord injury reduces the rate of skeletal muscle protein synthesis and increases protein breakdown, resulting in rapid muscle loss. The purpose of this study was to determine whether long-term paraplegia would eventually result in a downregulation of muscle mRNA and protein expression associated with both protein synthesis and breakdown. After 10 weeks of spinal cord transection, soleus muscle from 12 rats (6 sham-control, 6 paraplegic) was studied for mRNAs and proteins associated with protein synthesis and breakdown using real-time polymerase chain reaction and immunoblotting technique

Effect of Baduanjin exercise on primary osteoporosis: study protocol for randomized controlled trial.

BackgroundLack of exercise is often a major cause of chronic disease. Osteoporosis (OP) is a chronic disease with multifactorial co-morbidity. Baduanjin (BDJ) exercise may be a powerful tool for modifying risk factors. The aim is to provide more evidence about the effectiveness of BDJ exercise in improving pain and balance ability in patients with OP.MethodsIn the prospective randomized controlled trial, 160 participants will be recruited and randomized to the treatment group (BDJ exercise combined with Calcium carbonate and D3) or the control group (Calcium carbonate and D3) at 1:1 ratio. Par

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… to the Recommended Experiments for Biochemical Indicators of Bone Metabolism (2020 Expert Consensus, China) [ 20 ], the preliminary research results, and the literature survey, The serological indicators include Type I Procollagen N-terminal Propeptide (P1NP), β-collagen Degradation Product (β-CTX), Myostatin … control trial Visual analogue scale Bone mineral density Berg balance scale The timed “up and go” test Morse fall scale Five-times sit-to-stand test Dual energy X-ray absorptiometry Case report form Body mass index Type I procollagen N-terminal propeptide β-Collagen degradation product Myostatin …

Influence of the TGF-β Superfamily on Osteoclasts/Osteoblasts Balance in Physiological and Pathological Bone Conditions.

The balance between bone forming cells (osteoblasts/osteocytes) and bone resorbing cells (osteoclasts) plays a crucial role in tissue homeostasis and bone repair. Several hormones, cytokines, and growth factors-in particular the members of the TGF-β superfamily such as the bone morphogenetic proteins-not only regulate the proliferation, differentiation, and functioning of these cells, but also coordinate the communication between them to ensure an appropriate response. Therefore, this review focuses on TGF-β superfamily and its influence on bone formation and repair, through the regulation of

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… Then cells are incubated for 4–6 days with M-CSF (50 ng/mL) and RANKL (50 ng/mL) with or without myostatin (30 ng/mL) | Myostatin ↑ RANKL-induced expression of NFATc1; integrin αv, integrin β3, DC-STAMP and CTR Myostatin activates Smad2 to enhance RANKL-induced osteoclastogenesis NFATC1 and pSmad2 can … interact together favoring their nuclear translocation | No effect of Myostatin alone on osteoclast formation, apoptosis, and proliferation Myostatin + M-CSF/RANKL ↑ osteoclastogenesis (3.8-fold more osteoclasts after 4 days compared with M-CSF/RANKL control) ALK4/ALK5/ALK7 inhibitor ↓ number of osteoclasts …