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Relevant bibliographies by topics / Skeletal muscle dysfunction and wasting

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Academic literature on the topic 'Skeletal muscle dysfunction and wasting'

Author: Grafiati

Published: 10 January 2023

Last updated: 28 January 2023

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Journal articles on the topic "Skeletal muscle dysfunction and wasting"

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Hyatt, Hayden W., and Scott K. Powers. "Mitochondrial Dysfunction Is a Common Denominator Linking Skeletal Muscle Wasting Due to Disease, Aging, and Prolonged Inactivity." Antioxidants 10, no. 4 (April 11, 2021): 588. http://dx.doi.org/10.3390/antiox10040588.

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Skeletal muscle is the most abundant tissue in the body and is required for numerous vital functions, including breathing and locomotion. Notably, deterioration of skeletal muscle mass is also highly correlated to mortality in patients suffering from chronic diseases (e.g., cancer). Numerous conditions can promote skeletal muscle wasting, including several chronic diseases, cancer chemotherapy, aging, and prolonged inactivity. Although the mechanisms responsible for this loss of muscle mass is multifactorial, mitochondrial dysfunction is predicted to be a major contributor to muscle wasting in various conditions. This systematic review will highlight the biochemical pathways that have been shown to link mitochondrial dysfunction to skeletal muscle wasting. Importantly, we will discuss the experimental evidence that connects mitochondrial dysfunction to muscle wasting in specific diseases (i.e., cancer and sepsis), aging, cancer chemotherapy, and prolonged muscle inactivity (e.g., limb immobilization). Finally, in hopes of stimulating future research, we conclude with a discussion of important future directions for research in the field of muscle wasting.

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Man, William D. C., Paul Kemp, John Moxham, and Michael I. Polkey. "Exercise and muscle dysfunction in COPD: implications for pulmonary rehabilitation." Clinical Science 117, no. 8 (August 24, 2009): 281–91. http://dx.doi.org/10.1042/cs20080660.

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Skeletal muscle dysfunction in COPD (chronic obstructive pulmonary disease) patients, particularly of the quadriceps, is of clinical interest because it not only influences the symptoms that limit exercise, but may also contribute directly to poor exercise performance and health status, increased healthcare utilization, and mortality. Furthermore, unlike the largely irreversible impairment of the COPD lung, skeletal muscles represent a potential site to improve patients' level of function and quality of life. However, despite expanding knowledge of potential contributing factors and greater understanding of molecular mechanisms of muscle wasting, only one intervention has been shown to be effective in reversing COPD muscle dysfunction, namely exercise training. Pulmonary rehabilitation, an intervention based on individually tailored exercise training, has emerged as arguably the most effective non-pharmacological intervention in improving exercise capacity and health status in COPD patients. The present review describes the effects of chronic exercise training on skeletal muscles and, in particular, focuses on the known effects of pulmonary rehabilitation on the quadriceps muscle in COPD. We also describe the current methods to augment the effects of pulmonary rehabilitation and speculate how greater knowledge of the molecular pathways of skeletal muscle wasting may aid the development of novel pharmaceutical agents.

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Ignatieva, Elena, Natalia Smolina, Anna Kostareva, and Renata Dmitrieva. "Skeletal Muscle Mitochondria Dysfunction in Genetic Neuromuscular Disorders with Cardiac Phenotype." International Journal of Molecular Sciences 22, no. 14 (July 8, 2021): 7349. http://dx.doi.org/10.3390/ijms22147349.

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Mitochondrial dysfunction is considered the major contributor to skeletal muscle wasting in different conditions. Genetically determined neuromuscular disorders occur as a result of mutations in the structural proteins of striated muscle cells and therefore are often combined with cardiac phenotype, which most often manifests as a cardiomyopathy. The specific roles played by mitochondria and mitochondrial energetic metabolism in skeletal muscle under muscle-wasting conditions in cardiomyopathies have not yet been investigated in detail, and this aspect of genetic muscle diseases remains poorly characterized. This review will highlight dysregulation of mitochondrial representation and bioenergetics in specific skeletal muscle disorders caused by mutations that disrupt the structural and functional integrity of muscle cells.

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Man, William D. C., Paul Kemp, John Moxham, and Michael I. Polkey. "Skeletal muscle dysfunction in COPD: clinical and laboratory observations." Clinical Science 117, no. 7 (August 17, 2009): 251–64. http://dx.doi.org/10.1042/cs20080659.

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COPD (chronic obstructive pulmonary disease), although primarily a disease of the lungs, exhibits secondary systemic manifestations. The skeletal muscles are of particular interest because their function (or dysfunction) not only influences the symptoms that limit exercise, but may contribute directly to poor exercise performance. Furthermore, skeletal muscle weakness is of great clinical importance in COPD as it is recognized to contribute independently to poor health status, increased healthcare utilization and even mortality. The present review describes the current knowledge of the structural and functional abnormalities of skeletal muscles in COPD and the possible aetiological factors. Increasing knowledge of the molecular pathways of muscle wasting will lead to the development of new therapeutic agents and strategies to combat COPD muscle dysfunction.

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Conte, Elena, Elena Bresciani, Laura Rizzi, Ornella Cappellari, Annamaria De Luca, Antonio Torsello, and Antonella Liantonio. "Cisplatin-Induced Skeletal Muscle Dysfunction: Mechanisms and Counteracting Therapeutic Strategies." International Journal of Molecular Sciences 21, no. 4 (February 13, 2020): 1242. http://dx.doi.org/10.3390/ijms21041242.

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Among the severe side effects induced by cisplatin chemotherapy, muscle wasting is the most relevant one. This effect is a major cause for a clinical decline of cancer patients, since it is a negative predictor of treatment outcome and associated to increased mortality. However, despite its toxicity even at low doses, cisplatin remains the first-line therapy for several types of solid tumors. Thus, effective pharmacological treatments counteracting or minimizing cisplatin-induced muscle wasting are urgently needed. The dissection of the molecular pathways responsible for cisplatin-induced muscle dysfunction gives the possibility to identify novel promising therapeutic targets. In this context, the use of animal model of cisplatin-induced cachexia is very useful. Here, we report an update of the most relevant researches on the mechanisms underlying cisplatin-induced muscle wasting and on the most promising potential therapeutic options to preserve muscle mass and function.

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Ábrigo, Johanna, Alvaro A. Elorza, Claudia A. Riedel, Cristian Vilos, Felipe Simon, Daniel Cabrera, Lisbell Estrada, and Claudio Cabello-Verrugio. "Role of Oxidative Stress as Key Regulator of Muscle Wasting during Cachexia." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–17. http://dx.doi.org/10.1155/2018/2063179.

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Skeletal muscle atrophy is a pathological condition mainly characterized by a loss of muscular mass and the contractile capacity of the skeletal muscle as a consequence of muscular weakness and decreased force generation. Cachexia is defined as a pathological condition secondary to illness characterized by the progressive loss of muscle mass with or without loss of fat mass and with concomitant diminution of muscle strength. The molecular mechanisms involved in cachexia include oxidative stress, protein synthesis/degradation imbalance, autophagy deregulation, increased myonuclear apoptosis, and mitochondrial dysfunction. Oxidative stress is one of the most common mechanisms of cachexia caused by different factors. It results in increased ROS levels, increased oxidation-dependent protein modification, and decreased antioxidant system functions. In this review, we will describe the importance of oxidative stress in skeletal muscles, its sources, and how it can regulate protein synthesis/degradation imbalance, autophagy deregulation, increased myonuclear apoptosis, and mitochondrial dysfunction involved in cachexia.

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Hardee, Justin P., Ryan N. Montalvo, and James A. Carson. "Linking Cancer Cachexia-Induced Anabolic Resistance to Skeletal Muscle Oxidative Metabolism." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–14. http://dx.doi.org/10.1155/2017/8018197.

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Cancer cachexia, a wasting syndrome characterized by skeletal muscle depletion, contributes to increased patient morbidity and mortality. While the intricate balance between protein synthesis and breakdown regulates skeletal muscle mass, the suppression of basal protein synthesis may not account for the severe wasting induced by cancer. Therefore, recent research has shifted to the regulation of “anabolic resistance,” which is the impaired ability of nutrition and exercise to stimulate protein synthesis. Emerging evidence suggests that oxidative metabolism can regulate both basal and induced muscle protein synthesis. While disrupted protein turnover and oxidative metabolism in cachectic muscle have been examined independently, evidence suggests a linkage between these processes for the regulation of cancer-induced wasting. The primary objective of this review is to highlight the connection between dysfunctional oxidative metabolism and cancer-induced anabolic resistance in skeletal muscle. First, we review oxidative metabolism regulation of muscle protein synthesis. Second, we describe cancer-induced alterations in the response to an anabolic stimulus. Finally, we review a role for exercise to inhibit cancer-induced anabolic suppression and mitochondrial dysfunction.

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Furrer, Regula, and Christoph Handschin. "Muscle Wasting Diseases: Novel Targets and Treatments." Annual Review of Pharmacology and Toxicology 59, no. 1 (January 6, 2019): 315–39. http://dx.doi.org/10.1146/annurev-pharmtox-010818-021041.

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Adequate skeletal muscle plasticity is an essential element for our well-being, and compromised muscle function can drastically affect quality of life, morbidity, and mortality. Surprisingly, however, skeletal muscle remains one of the most under-medicated organs. Interventions in muscle diseases are scarce, not only in neuromuscular dystrophies, but also in highly prevalent secondary wasting pathologies such as sarcopenia and cachexia. Even in other diseases that exhibit a well-established risk correlation of muscle dysfunction due to a sedentary lifestyle, such as type 2 diabetes or cardiovascular pathologies, current treatments are mostly targeted on non-muscle tissues. In recent years, a renewed focus on skeletal muscle has led to the discovery of various novel drug targets and the design of new pharmacological approaches. This review provides an overview of the current knowledge of the key mechanisms involved in muscle wasting conditions and novel pharmacological avenues that could ameliorate muscle diseases.

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Silva, Kleiton Augusto Santos, Thaysa Ghiarone, Kathy Schreiber, DeAna Grant, Tommi White, Madlyn I. Frisard, Sergiy Sukhanov, Bysani Chandrasekar, Patrice Delafontaine, and Tadashi Yoshida. "Angiotensin II suppresses autophagy and disrupts ultrastructural morphology and function of mitochondria in mouse skeletal muscle." Journal of Applied Physiology 126, no. 6 (June 1, 2019): 1550–62. http://dx.doi.org/10.1152/japplphysiol.00898.2018.

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Angiotensin II (ANG II)-induced skeletal muscle wasting is characterized by activation of the ubiquitin-proteasome system. However, the potential involvement of proteolytic system macroautophagy/autophagy in this wasting process remains elusive. Autophagy is precisely regulated to maintain cell survival and homeostasis; thus its dysregulation (i.e., overactivation or persistent suppression) could lead to detrimental outcomes in skeletal muscle. Here we show that infusion of ANG II for 7 days in male FVB mice suppressed autophagy in skeletal muscle. ANG II blunted microtubule-associated protein 1 light chain 3B (LC3B)-I-to-LC3B-II conversion (an autophagosome marker), increased p62/SQSTM1 (an autophagy cargo receptor) protein expression, and decreased the number of autophagic vacuoles. ANG II inhibited UNC-51-like kinase 1 via inhibition of 5′-AMP-activated kinase and activation of mechanistic target of rapamycin complex 1, leading to reduced phosphorylation of beclin-1Ser14 and Autophagy-related protein 14Ser29, suggesting that ANG II impairs autophagosome formation in skeletal muscle. In line with ANG II-mediated suppression of autophagy, ANG II promoted accumulation of abnormal/damaged mitochondria, characterized by swelling and disorganized cristae and matrix dissolution, with associated increase in PTEN-induced kinase 1 protein expression. ANG II also reduced mitochondrial respiration, indicative of mitochondrial dysfunction. Together, these results demonstrate that ANG II reduces autophagic activity and disrupts mitochondrial ultrastructure and function, likely contributing to skeletal muscle wasting. Therefore, strategies that activate autophagy in skeletal muscle have the potential to prevent or blunt ANG II-induced skeletal muscle wasting in chronic diseases. NEW & NOTEWORTHY Our study identified a novel mechanism whereby angiotensin II (ANG II) impairs mitochondrial energy metabolism in skeletal muscle. ANG II suppressed autophagosome formation by inhibiting the UNC-51-like kinase 1(ULK1)-beclin-1 axis, resulting in accumulation of abnormal/damaged and dysfunctional mitochondria and reduced mitochondrial respiratory capacity. Therapeutic strategies that activate the ULK1-beclin-1 axis have the potential to delay or reverse skeletal muscle wasting in chronic diseases characterized by increased systemic ANG II levels.

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Leduc-Gaudet, Jean-Philippe, Dominique Mayaki, Olivier Reynaud, Felipe E. Broering, Tomer J. Chaffer, Sabah N. A. Hussain, and Gilles Gouspillou. "Parkin Overexpression Attenuates Sepsis-Induced Muscle Wasting." Cells 9, no. 6 (June 11, 2020): 1454. http://dx.doi.org/10.3390/cells9061454.

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Sepsis elicits skeletal muscle weakness and fiber atrophy. The accumulation of injured mitochondria and depressed mitochondrial functions are considered as important triggers of sepsis-induced muscle atrophy. It is unclear whether mitochondrial dysfunctions in septic muscles are due to the inadequate activation of quality control processes. We hypothesized that overexpressing Parkin, a protein responsible for the recycling of dysfunctional mitochondria by the autophagy pathway (mitophagy), would confer protection against sepsis-induced muscle atrophy by improving mitochondrial quality and content. Parkin was overexpressed for four weeks in the limb muscles of four-week old mice using intramuscular injections of adeno-associated viruses (AAVs). The cecal ligation and perforation (CLP) procedure was used to induce sepsis. Sham operated animals were used as controls. All animals were studied for 48 h post CLP. Sepsis resulted in major body weight loss and myofiber atrophy. Parkin overexpression prevented myofiber atrophy in CLP mice. Quantitative two-dimensional transmission electron microscopy revealed that sepsis is associated with the accumulation of enlarged and complex mitochondria, an effect which was attenuated by Parkin overexpression. Parkin overexpression also prevented a sepsis-induced decrease in the content of mitochondrial subunits of NADH dehydrogenase and cytochrome C oxidase. We conclude that Parkin overexpression prevents sepsis-induced skeletal muscle atrophy, likely by improving mitochondrial quality and contents.

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Dissertations / Theses on the topic "Skeletal muscle dysfunction and wasting"

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Zhang, Yan. "Cytokines and skeletal muscle wasting." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ47124.pdf.

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Tarabees, Reda Zakaria Ibrahim. "Endotoxin induced muscle wasting in avian and murine skeletal muscle." Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/13001/.

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This project was aimed to elucidate the sub-cellular and molecular regulation of Lipopolysaccharide (LPS) induced muscle protein turnover (protein synthesis (PS) and protein degradation) in two in vitro models, C2C12 murine myotubes and avian primary skeletal muscle cell line. In addition, the effect of natural challenge of chicken with Salmonella serotypes gallinarium or Enteritidis on mRNA expression levels in skeletal muscle was assessed. LPS (1 μgml-1) transiently decreased PS rate by 50% compared with control cells. This effect was mediated via decreased phosphorylation of translation initiation mediators (p70S6K, 4E-BP1 and eIF-4E). This effect was preceded by decreased Akt and mTOR phosphorylation. Although, LPS significantly increased p38, Erk1/2 and their down stream target Mnk1, however, this effect was not sufficient to abolish LPS-induced decreased PS. The role of Akt and MAPKs (p38 or Erk1/2) was verified using specific pathway inhibitors. Inhibition of Akt by LY0294002 (PI3-K/Akt inhibitor) dramatically decreased PS by 80% compared with control cells. Incubation of C2C12 myotubes with SB203580 (p38 inhibitor) or with PD098059 (MEK/Erk inhibitor) alone significantly decreased the PS rate at the 3 h time point by -63 ± 12.48% and -64 ± 5.05% respectively compared with control cells (P < 0.01). In contrast, LPS (1 μgml-1) significantly increased the chymotrypsin-like enzyme at all the time points. This effect was preceded by a significant increase in the IkB-α phosphorylation and nuclear translocation of NF-kB, and significant increase in TNF-α, atrogin-1, MuRF1 and TLR4 mRNA expression. Of note, increased atrogin-1 mRNA is the prominent feature of our septic model. The data presented in chapter 4 and 5 showed that, there is no absolute correlation between the expression levels of atrogens (atrogin-1 and MuRF1) and the overall proteolytic activity in LPS-stimulated C2C12 myotubes. The beneficial roles of the curcumin were evaluated LPS-stimulated C2C12 myotubes for 3 h. Incubation of C2C12 myotubes with LPS (1 μgml-1) and curcumin (25 μM) significantly decreased the LPS-induced chymotrypsin-like enzyme activity. This effect was mediated via decreased p38 and IkB-α phosphorylation. Although, curcumin blocked LPS-induced decreased Akt and p70S6K phosphorylation and significantly increased Erk1/2 phosphorylation, however, curcumin still had no effect on LPS-induced decreased protein synthesis. The effect of the LPS on the muscle protein turnover in the avian primary skeletal muscle was summarised in chapter (7). Incubation of avian primary skeletal cells with LPS (1 μgml-1) for 3 h, significantly decreased the proteasomal activity and increased PS rate. The difference in response to LPS between C2C12 myotubes and avian primary skeletal muscle cells could be attributed to the different incubation parameters mainly the presence of insulin in case of avian primary cells. Finally, the effect of natural challenge of chicken with S. Gallinarum or S. Enteritidis on skeletal muscle mRNA expression was summarised in chapter 9. Natural challenge of chicken with S. Gallinarum or S. Enteritidis had no effect on the expression of many atrophic genes in chicken skeletal muscle (gastrocnemius and pectoral muscle). The data collected from this project showed that, LPS is a strong catabolic stimulus significantly decreased PS along with increased protein breakdown rates in skeletal muscle. This effect was mediated via two main pathways PI3-K/Akt and MAPKs (p38 or Erk1/2) and the cross talk between them is exists. The better understanding of these signalling cascades and their cross talk will be the starting point for developing the appropriate and safe therapeutic intervention in order to decrease the sepsis-induced muscle proteolysis.

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Puthucheary, Z. A. "Acute skeletal muscle wasting in the critically ill." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1425686/.

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Introduction: Critical illness survivors demonstrate skeletal muscle wasting with associated functional impairment. I prospectively characterised this process, and defined the pathogenic roles of altered protein synthesis and degradation. Methods: Critically ill patients (n=63, 59% male, age 54.7±18.0 years, APACHE II score 23.5±6.5) were recruited <24 hours following intensive care admission. Muscle loss trajectory was determined through serial ultrasound measurement of rectus femoris cross-sectional area (RFCSA) and, in a subset, quantification of myofibre area (FibreCSA) and protein/DNA ratio. Histopathological analysis was performed. Muscle protein synthesis and breakdown rates were determined and respective signalling pathways examined. Results: RFCSA decreased significantly, (-17.7±12.1%, [p<0.001]), underestimating muscle loss determined by FibreCSA (-10.3±10.9% vs.-17.5±30.2%, p=0.31), or protein/DNA ratio (-10.3±10.9% vs. -29.5±41.5%, p=0.03). Fall in RFCSA was greater in multi- than single-organ failure (-21.5±10.5% vs. - 7.2± 9.7%, p <0.0001), even by day 3 (-8.7±16.3% vs. -1.8± 9.6%, p<0.01). Myofibre necrosis occurred in >50% (20/37) of subjects. Protein synthesis was depressed to levels observed in fasted controls (0.035±0.018%/hr vs. 0.039±0.011%/hr, p=0.57), and increased by day 7 (0.076±0.066%/hr, p=0.03) to levels associated with fed controls (0.065+0.018%/hr, p=0.30,) independent of nutritional load. Protein breakdown remained elevated throughout (8.5±5.7 to 10.6±5.7mmol phe/min/IBW, p=0.4).Principal component analysis of intracellular signalling supported a programme of increased breakdown (r=-0.83, p=0.005) and depressed synthesis (r=-.69, p=0.041). Conclusions: Early rapid skeletal muscle wasting occurs in critical illness, is greatest in those with multi-organ failure, and results from suppression of protein synthesis and increases in catabolism. These effects are independent of feeding and are commonly associated with myonecrosis.

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Pickering, Warren Paul. "Regulation of metabolic acidosis-induced skeletal muscle wasting." Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/30504.

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This work aims to investigate metabolic acidosis induced skeletal muscle protein wasting, and the inter-relationships between: metabolic acidosis, glucocorticoids (GC), and the ubiquitin proteasome system in this process.;Experiments were undertaken using three key themes and models: 1. The role of glucocorticoids and apoptosis in the process of protein degradation (PD) in L6G8C5 myoblasts in a cell culture system of metabolic acidosis utilizing dexamethasone and the glucocorticoid antagonist RU38486. Stimulation of PD in these cells by acid and GC does not appear to be an artefact of apoptosis or dedifferentiation, but differentiation state does determine whether PD responds spontaneously to acid or (as in vivo) only does so in the presence of GC. 2. The ability of RU38486 to pharmacologically antagonize the suggested permissive effect of glucocorticoid in an in vivo model of acidosis-induced muscle wasting. RU38486 did not prevent the acidosis-induced muscle wasting in this model despite demonstration of significant GC receptor blockade. 3. The role of the ATP-dependent ubiquitin proteasome system in the malnutrition of patients treated by peritoneal dialysis. When serum bicarbonate increased in these patients weight and body mass index increased significantly as did plasma BCAA. Muscle levels of ubiquitin mRNA decreased significantly; serum tumour necrosis factor-a also decreased. These results indicate that even a small correction of serum bicarbonate improves nutritional status, and provide evidence for down-regulation of BCAA degradation and muscle proteolysis via the ubiquitin proteasome system. Whether acidosis and inflammatory cytokines (such as TNF-alpha) interact to impair nutrition remains to be determined.

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Aydogdu, Tufan. "STAT3 Regulation of Skeletal Muscle Wasting in Cancer Cachexia." Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_dissertations/652.

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Cachexia is a highly complex syndrome identified by metabolic, hormonal and cytokine-related abnormalities, but can be shortly characterized as accelerated skeletal muscle and adipose tissue loss in the context of a chronic inflammatory response. Cachexia is a debilitating complication of several diseases such as AIDS, sepsis, diabetes, renal failure, burn injury and cancer. Cachexia is responsible for 25-30% of cancer patient deaths. One of the most obvious outcomes of cancer cachexia is the redistribution of the total protein content, namely the depletion of skeletal muscle protein levels and increase in the acute phase response protein levels as a response to tissue injury. Although the plasticity of muscle mass and utility of skeletal muscle as a protein source are known facts, there have not been many studies concerning the mechanism of conversion of skeletal muscle proteins to other protein forms, for which the organism has greater need. IL-6 and activation of the acute phase response have been linked to cancer cachexia. However, IL-6 is generally not thought to signal directly on skeletal muscle and to date no studies have manipulated the STAT3 pathway for regulating skeletal muscle mass. Our data demonstrate direct action of IL-6 on activation of the STAT3 and acute phase response pathway at the skeletal muscle. In addition, our observations that STAT3 is broadly activated in cachexia and that STAT3 activation is sufficient and necesssary to induce muscle wasting are also novel. Thus, these studies define a new pathway leading to muscle wasting, which can be a potential target for reversing muscle wasting in cancer cachexia. Successful inhibition of skeletal muscle wasting and other metabolic derangements of cachexia will increase quality of life and survival of a significant fraction of cancer patients.

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Antunes, Diana Sofia Ribeiro Duarte. "Lipidomic and proteomic in cancer-related skeletal muscle wasting." Master's thesis, Universidade de Aveiro, 2013. http://hdl.handle.net/10773/11613.

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Mestrado em Bioquímica Clínica
A caquexia associada ao cancro é uma condição fisiopatológica complexa caraterizada por acentuada perda de massa muscular.Recentemente, esta situação foi associada à disfunção mitocondrial. A relação e o papel do proteoma e lipidoma mitocondrial e a funcionalidade deste organelo permanece pouco compreendida, em particular no contexto do catabolismo muscular associado ao cancro. No sentido de melhor compreender os mecanismos moleculares subjacentes às alterações no músculo esquelético na caquexia associada ao cancro, utilizaram-se 23 ratos Wistar divididos aleatoriamente em dois grupos: com cancro da bexiga induzido pela exposição durante 20 semanas a N-butil-N-(4-hidroxibutil)-nitrosamina (grupo BBN, n=13) ou saudáveis (CONT, n=10). No final do protocolo verificou-se que os animais do grupo BBN apresentavam uma perda significativa de peso corporal e de massa muscular. Também foi observado uma diminuição da atividade da fosforilação oxidativa de mitocôndrias isoladas do músculo gastrocnemius. a qual foi acompanhada por alterações do perfil de fosfolípidos (PL) da mitocôndria. A alteração do lipidoma mitocondrial caraterizou-se pelo aumento do teor relativo de fosfatidilcolinas (PC) e fosfatidilserina (PS) e uma redução no teor relativo de cardiolipina (CL), ácido fosfatídico (PA), fosfatidilglicerol (PG) e fosfatidilinositol (PI). A análise realizada por GC-FID e HPLC-ESI-MS evidenciou ainda um aumento de ácidos gordos polinsaturados, com um aumento destacado de C22:6 em PC, PE e PS. A diminuição de CL foi acompanhada por diminuição na expressão de citocromo c e aumento da razão Bax/Bcl2, sugestivo de maior suscetibilidade à apoptose e stress oxidativo. Embora em níveis mais elevados, a UCP-3 não parece proteger as proteínas mitocondriais da lesão oxidativa atendendo ao aumento do teor de proteínas carboniladas. Em conclusão, a remodelação de PL da mitocôndria parece estar associada à disfunção da OXPHOS e, consequentemente, do catabolismo muscular associado ao cancro.
Cancer cachexia (CC) is a complex pathophysiological condition characterized by a marked muscle wasting. Recently, this situation has been associated to mitochondrial dysfunction. The interplay and role of mitochondrial proteome and lipidome and also the functionality of this organelle remains poorly understood in the context of cancer-related muscle wasting. To better understand the molecular mechanisms underlying skeletal muscle wasting, 23 Wistar rats were randomly divided in two groups: animals with bladder cancer induced by the exposition to N-butyl-N-(4-hydroxybutyl)-nitrosamine for 20 weeks (BBN, n=13) or healthy ones (CONT, n=10). At the end of the experimental protocol, BBN animals demonstrated a significant body weight and muscle mass loss and was also observed an decreased activity of oxidative phosphorylation in mitochondria isolated from gastrocnemius muscle, which was accompanied by alterations of this organelle’s phospholipids (PL) profile. The mitochondrial lipidome alterations were characterized by an increase of the relative content of phosphatidylcholines (PC) and phosphatidylserine (PS) and a decrease of cardiolipin (CL), phosphatidic acid (PA), phosphatidylglycerol (PG) and phosphatidylinositol (PI). GC-FID and HPLC-ESI-MS analysis also showed an increase of polyunsaturated fatty acids, particularly of C22:6 in PC, PE and PS. The observed decrease in CL class was accompanied by a decrease in the expression of cytochrome c, and an increase of the ratio Bax/Bcl-2, suggestive of a greater susceptibility to apoptosis and oxidative stress. Although in higher levels, UCP-3 does not seem to protect mitochondrial proteins from oxidative damage considering the increased content of carbonylated protein. In conclusion, the PL remodeling seems to be associated to OXPHOS dysfunction and consequently to muscle catabolism associated with cancer.

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Aare, Sudhakar Reddy. "Intensive Care Unit Muscle Wasting : Skeletal Muscle Phenotype and Underlying Molecular Mechanisms." Doctoral thesis, Uppsala universitet, Klinisk neurofysiologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-180374.

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Acute quadriplegic myopathy (AQM), or critical illness myopathy, is a common debilitating acquired disorder in critically ill intensive care unit (ICU) patients characterized by generalized muscle wasting and weakness of limb and trunk muscles. A preferential loss of the thick filament protein myosin is considered pathognomonic of this disorder, but the myosin loss is observed relatively late during the disease progression. In attempt to explore the potential role of factors considered triggering AQM in sedated mechanically ventilated (MV) ICU patients, we have studied the early effects, prior to the myosin loss, of neuromuscular blockade (NMB), corticosteroids (CS) and sepsis separate or in combination in a porcine experimental ICU model. Specific interest has been focused on skeletal muscle gene/protein expression and regulation of muscle contraction at the muscle fiber level. This project aims at improving our understanding of the molecular mechanisms underlying muscle specific differences in response to the ICU intervention and the role played by the different triggering factors. The sparing of masticatory muscle fiber function was coupled to an up-regulation of heat shock protein genes and down-regulation of myostatin are suggested to be key factors in the relative sparing of masticatory muscles. Up-regulation of chemokine activity genes and down-regulation of heat shock protein genes play a significant role in the limb muscle dysfunction associated with sepsis. The effects of corticosteroids in the development of limb muscle weakness reveals up-regulation of kinase activity and transcriptional regulation genes and the down-regulation of heat shock protein, sarcomeric, cytoskeletal and oxidative stress responsive genes. In contrast to limb and craniofacial muscles, the respiratory diaphragm muscle responded differently to the different triggering factors. MV itself appears to play a major role for the diaphragm muscle dysfunction. By targeting these genes, future experiments can give an insight into the development of innovative treatments expected at protecting muscle mass and function in critically ill ICU patients.

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Moore, Tamara W. I. "The role of USP19 in denervation induced skeletal muscle wasting." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=94923.

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Skeletal muscle wasting can be a fatal complication of many diseases, such as cancer, AIDS and neuromuscular disorders. During wasting, the ubiquitin-proteasome system (UPS) is the primary pathway for the catabolism of myofibrillar proteins. Many studies have explored the importance of enzymes mediating the conjugation of ubiquitin to muscle proteins. However, the role of deubiquitinating enzymes in skeletal muscle wasting is poorly understood. Our laboratory previously identified USP19 as a deubiquitinating enzyme which is upregulated in response to atrophic stimuli in vivo and is capable of indirectly regulating the expression of myofibrillar proteins in muscle cells in vitro. However, the role of USP19 during skeletal muscle wasting in vivo remains unexplored. To address this question, I have characterized the phenotype of USP19 KO mice and determined the effects of denervation induced wasting of hindlimb muscles of USP19 KO mice by measuring various anatomical and structural parameters. Denervation stimulus was chosen to minimize number of animals used since control and treated limbs are within the same animal. USP19 KO mice had slightly heavier gastrocnemius muscle (GAS) mass than WT mice, with a trend towards a larger fiber size and higher protein content. After denervation, the skeletal muscle mass of KO mice is 30% heavier than that of denervated WT mice in both the tibialis anterior (TA) and GAS muscle. This significant sparing is correlated with KO having 30% more protein than WT in GAS muscles, after denervation. The level of the myofibrillar protein tropomyosin was significantly higher in denervated KO GAS than in denervated WT GAS, consistent with previous USP19 siRNA studies in rat skeletal muscle cells. Although, structural analysis of denervated GAS fiber reveals a small but significant sparing in the fiber size of KO mice as compared to WT mice, this difference only accounts for 5% of the mass sparing observed in KOs. Loss of neural stimulation
L'atrophie musculaire est une grave complication qui peut être fatale dans plusieurs maladies comme le cancer, le SIDA ou les maladies neuromusculaires. Le système ubiquitine-protéasome (UPS) est le mécanisme le plus impliqué dans la dégradation des protéines myofibrillaires durant l'atrophie. Plusieurs études ont démontré l'importance de certaines enzymes catalysant la conjugaison de l'ubiquitine aux protéines musculaires. Parcontre, le rôle des enzymes de déubiquitination durant l'atrophie musculaire est encore très peu connu. Notre laboratoire a précédemment identifié USP19, une enzyme de déubiquitination, qui est régulée à la hausse en réponse à plusieurs stimuli d'atrophie musculaire in vivo et qui est aussi capable de réguler indirectement des protéines myofibrillaires dans des cellules musculaires in vitro. Toutefois, le rôle de USP19 dans l'atrophie musculaire in vivo est encore inconnu. Afin d'aborder cette question, j'ai caractérisé le phénotype de souris dont le gène USP19 a été inactivé (KO) et j'ai déterminé les effets d'une dénervation des muscles de la patte postérieur sur ces souris KO en mesurant divers paramètres anatomiques et structuraux. Les souris USP19 KO possèdent une masse du muscle gastrocnemius (GAS) légèrement plus grande que les souris contrôles (WT) avec une tendance vers des fibers plus grosses et un contenu protéique plus élevé. Après dénervation, les muscles squelletiques des souris KO étaient 30% plus lourds que ceux des souris WT et ce dans le GAS ainsi que dans le tibialis postérieur (TA). Cette économie significative corrèle bien avec une augmentation de 30% du contenu protéique dans les muscles KO (GAS) comparé aux muscles WT, après dénervation. Aussi, les niveaux de la protéine myofibrillaire tropomyosine étaient significativement plus élevés dans le GAS KO que dans que dans le GAS WT, après dénervation, ce qui est consistant avec des études postérieures de siRNA

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Rosa, Hannah Sophia. "Pathogenesis of mitochondrial dysfunction in skeletal muscle." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3969.

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Mitochondrial diseases are amongst the most prevalent genetic disorders, however little is known about genetic and cellular mechanisms behind disease pathogenesis and progression. Elucidating such mechanisms can help identify targets for novel therapeutic measures and improve patient care by informing the implementation of clinical regimens and providing clearer information on prognoses. This project aims to improve the understanding of the molecular mechanisms behind the pathogenesis of mitochondrial dysfunction in muscle and the genetic and biochemical changes occurring over time in patients with mitochondrial disease. Firstly, a longitudinal study combines immunofluorescent and molecular genetic techniques to assess biochemical and genetic changes over time in serial skeletal muscle biopsies from patients with m.3243A > G or single, large-scale mtDNA deletions, the two largest groups in the MRC Centre Mitochondrial Disease Patient Cohort. Further investigation into the relationship between the genetic and biochemical defects in patients with single, large-scale mtDNA deletions is carried out by applying a single-fibre approach. Here, muscle fibres are classified by their biochemical defect and laser microdissected for genetic analysis to determine deletion level and mtDNA copy number. These studies find that: (i) changes to mutation level, mtDNA copy number and biochemical defect occur over time in skeletal muscle of mitochondrial disease patients; (ii) these changes are inconsistent in magnitude and direction across groups of patients and (iii) the biochemical threshold for deficiency is affected by the size and location of single, large-scale mtDNA deletions. In addition, a real time PCR assay for the quantification of mitochondrial DNA copy number from homogenate tissue has been optimised to improve accuracy through the use of additional gene markers.

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Pattison, J. Scott. "Understanding muscle wasting through studies of gene expression and function." Free to MU Campus, others may purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p3164536.

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Books on the topic "Skeletal muscle dysfunction and wasting"

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Pinheiro, Carlos Hermano J., and Lucas Guimarães-Ferreira, eds. Frontiers in Skeletal Muscle Wasting, Regeneration and Stem Cells. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-832-0.

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Chiou, Michael, and John Bach. Physical Medicine Interventions for Skeletal and Cardiac Muscle Dysfunction. Chiou, Michael, 2021.

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Chiou, Michael, and John Bach. Physical Medicine Interventions for Skeletal and Cardiac Muscle Dysfunction. Chiou, Michael, 2021.

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Hall, Andrew, and Shamima Rahman. Mitochondrial diseases and the kidney. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0340.

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Mitochondrial disease can affect any organ in the body including the kidney. As increasing numbers of patients with mitochondrial disease are either surviving beyond childhood or being diagnosed in adulthood, it is important for all nephrologists to have some understanding of the common renal complications that can occur in these individuals. Mitochondrial proteins are encoded by either mitochondrial or nuclear DNA (mtDNA and nDNA, respectively); therefore, disease causing mutations may be inherited maternally (mtDNA) or autosomally (nDNA), or can arise spontaneously. The commonest renal phenotype in mitochondrial disease is proximal tubulopathy (Fanconi syndrome in the severest cases); however, as all regions of the nephron can be affected, from the glomerulus to the collecting duct, patients may also present with proteinuria, decreased glomerular filtration rate, nephrotic syndrome, water and electrolyte disorders, and renal tubular acidosis. Understanding of the relationship between underlying genotype and clinical phenotype remains incomplete in mitochondrial disease. Proximal tubulopathy typically occurs in children with severe multisystem disease due to mtDNA deletion or mutations in nDNA affecting mitochondrial function. In contrast, glomerular disease (focal segmental glomerulosclerosis) has been reported more commonly in adults, mainly in association with the m.3243A<G point mutation. Co-enzyme Q10 (CoQ10) deficiency has been particularly associated with podocyte dysfunction and nephrotic syndrome in children. Underlying mitochondrial disease should be considered as a potential cause of unexplained renal dysfunction; clinical clues include lack of response to conventional therapy, abnormal mitochondrial morphology on kidney biopsy, involvement of other organs (e.g. diabetes, cardiomyopathy, and deafness) and a maternal family history, although none of these features are specific. The diagnostic approach involves acquiring tissue (typically skeletal muscle) for histological analysis, mtDNA screening and oxidative phosphorylation (OXPHOS) complex function tests. A number of nDNA mutations causing mitochondrial disease have now been identified and can also be screened for if clinically indicated. Management of mitochondrial disease requires a multidisciplinary approach, and treatment is largely supportive as there are currently very few evidence-based interventions. Electrolyte deficiencies should be corrected in patients with urinary wasting due to tubulopathy, and CoQ10 supplementation may be of benefit in individuals with CoQ10 deficiency. Nephrotic syndrome in mitochondrial disease is not typically responsive to steroid therapy. Transplantation has been performed in patients with end-stage kidney disease; however, immunosuppressive agents such as steroids and tacrolimus should be used with care given the high incidence of diabetes in mitochondrial disease.

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Hough, Catherine L. The Impact of Critical Illness on Skeletal Muscle Structure. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0034.

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Patients with critical illness are at risk of profound weakness and skeletal muscle loss, and recovery is marked by prolonged physical functional impairment in many survivors. Muscle and nerve abnormalities found in critically ill patients include loss of muscle mass, muscle membrane inexcitability, polyneuropathy, mitochondrial dysfunction with bioenergetic failure, as well as changes in skeletal muscle structure. The most common histological abnormalities are atrophy of both type I and II fibres and thick filament loss; muscle necrosis is less common. While recent studies have illuminated the pathogenesis of critical illness myopathy, additional high-quality translational research is needed to identify targets for therapeutic intervention.

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Chiou, Michael, and John Bach. Physical Medicine Interventions for Skeletal and Cardiorespiratory Muscle Dysfunction: The Conditions and Their Medical and Surgical Management. Chiou, Michael, 2020.

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Stevens, Robert D. Introduction: Biological Mechanisms of Injury and Repair. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0026.

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Chapter 26 is an introduction to devoted to biological mechanisms underpinning organ dysfunction and repair in critical illness, and how research has generated fundamental insights into the biology of conditions, such as sepsis and ARDS, and has suggested important new therapeutic paradigms. It also specifically addresses issues surrounding genetic susceptibility, cognitive deficiency, frailty, myocardial ischaemia, muscle wasting, sepsis-associated encephalopathy (SAE), CIP, and structural muscle alterations.

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Hart, Nicholas, and Tarek Sharshar. Diagnosis, assessment, and management of ICU-acquired weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0248.

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Intensive care unit-acquired weakness (ICU-AW) is the term applied to generalized skeletal muscle weakness developed as a result of critical illness. This condition adversely affects up to three-quarters of patients admitted to the intensive care unit and it is associated with risk factors such as illness severity and duration of mechanical ventilation. Using detailed electrophysiological tests and histological muscle sampling, ICU-AW can be classified as a neuropathy, myopathy, or a neuromyopathy. However, this detailed approach is generally only required when there is diagnostic uncertainty and a simple test to diagnose ICU-AW utilizing manual muscle testing and the Medical Research Council (MRC) sumscore are more commonly employed. Nonetheless, short- and long-term outcomes associated with developing ICU-AW using MRC sumscore, have been reported. Intervention exercise therapy and rehabilitation strategies are required to minimize the effects of developing of skeletal muscle wasting.

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Manlapaz, Mariel, and Perin Kothari. Neuromuscular Disorders and Anesthesia. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0029.

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The various neuromuscular diseases present with different airway, cardiovascular, pulmonary, and anesthetic considerations. It is useful to categorize these different diseases into nerve, neuromuscular junction, and primary muscle diseases. Understanding their pathophysiology is paramount in choosing the right anesthetic drugs (for example, depolarizing versus nondepolarizing and regional versus general anesthesia). Knowing their manifestations such as autonomic dysfunction, skeletal/cardiac/smooth/bulbar muscle involvement, or tendency for tonic contraction, allows for expectant perioperative management. Finally appreciating their association with certain disease states such as malignant hyperthermia or endocrine dysfunction can prevent complications. A brief review of myotonic dystrophy is presented here, followed by a brief summary of anesthetic considerations for various neuromuscular diseases.

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Yaqoob, Muhammad M. Acidosis in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0148.

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Metabolic acidosis becomes increasingly common as chronic kidney disease progresses. It is associated with a number of complications, including bone disease, altered protein synthesis and degradation, skeletal muscle wasting, and lately progressive glomerular filtration rate loss. Experimental and clinical studies suggest a role for alkali therapy to lessen these complications. Recent controlled studies support this notion, and suggest that correction of metabolic acidosis in patients with chronic kidney disease slows the rate of decline of renal function and the development of end-stage renal disease, although more definitive evidence is needed on the long-term benefits of alkali therapy, type of alkali supplements, and the optimal level of serum bicarbonate.

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Book chapters on the topic "Skeletal muscle dysfunction and wasting"

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Caron, Marc-André, Marie-Eve Thériault, Richard Debigaré, and François Maltais. "Skeletal Muscle Dysfunction." In Chronic Obstructive Pulmonary Disease, 137–59. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60761-673-3_9.

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Buck, M., and M. Chojkier. "Oxidative stress and muscle wasting of cachexia." In Oxidative Stress in Skeletal Muscle, 273–82. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8958-2_17.

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Herbert, Eric K., Saul R. Herbert, and Karl E. Herbert. "Skeletal Muscle Mitochondrial Toxicity." In Mitochondrial Dysfunction Caused by Drugs and Environmental Toxicants, 111–31. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119329725.ch8.

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Gosselin, Luc E. "Skeletal Muscle Collagen: Age, Injury and Disease." In Sarcopenia – Age-Related Muscle Wasting and Weakness, 159–72. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9713-2_8.

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O’Connell, Kathleen, Philip Doran, Joan Gannon, Pamela Donoghue, and Kay Ohlendieck. "Proteomic and Biochemical Profiling of Aged Skeletal Muscle." In Sarcopenia – Age-Related Muscle Wasting and Weakness, 259–87. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9713-2_12.

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Delbono, Osvaldo. "Excitation-Contraction Coupling Regulation in Aging Skeletal Muscle." In Sarcopenia – Age-Related Muscle Wasting and Weakness, 113–34. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9713-2_6.

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Roth, Stephen M. "Genetic Variation and Skeletal Muscle Traits: Implications for Sarcopenia." In Sarcopenia – Age-Related Muscle Wasting and Weakness, 223–57. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9713-2_11.

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Hepple, Russell T. "Alterations in Mitochondria and Their Impact in Aging Skeletal Muscle." In Sarcopenia – Age-Related Muscle Wasting and Weakness, 135–58. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9713-2_7.

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Muoio, Deborah M., and Timothy R. Koves. "Lipid-Induced Metabolic Dysfunction in Skeletal Muscle." In Novartis Foundation Symposia, 24–46. Chichester, UK: John Wiley & Sons, Ltd, 2007. http://dx.doi.org/10.1002/9780470985571.ch4.

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Russell, Aaron P., and Bertrand Lèger. "Age-Related Changes in the Molecular Regulation of Skeletal Muscle Mass." In Sarcopenia – Age-Related Muscle Wasting and Weakness, 207–21. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9713-2_10.

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Conference papers on the topic "Skeletal muscle dysfunction and wasting"

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Burke, Hannah, C. Mirella Spalluto, Doriana Cellura, Karl J. Staples, and Tom M. A. Wilkinson. "Role of exosomal microRNA in driving skeletal muscle wasting in COPD." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa2930.

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Polverino, F., B. D'Agostino, C. Santoriello, and M. Polverino. "Cytochrome Oxidase Activity and Skeletal Muscle Dysfunction in COPD." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4205.

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Poberezhets, Vitalii, Szymon Skoczyński, Anna Demchuk, Aleksandra Oraczewska, Ewelina Tobiczyk, Yuriy Mostovoy, and Adam Barczyk. "Skeletal muscle dysfunction among COPD patients in Eastern Europe." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2476.

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maurya, abhishek, ankit patel, and Atul Tiwari. "Evaluation of Skeletal Muscle Dysfunction in COPD OSA Overlap Syndrome." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2312.

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Poberezhets, Vitalii, Yuriy Mostovoy, and Hanna Demchuk. "Features of skeletal muscle dysfunction in COPD patients with obesity." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa684.

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Krall, J. T. W., L. Belfield, L. D. Purcell, R. D. Stapleton, M. E. Poynter, M. Toth, C. Liu, K. Gibbs, and D. C. Files. "Leukocyte Kinetics in Acute Lung Injury (ALI)-Associated Skeletal Muscle Wasting and Recovery." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2659.

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Files, D. Clark, Laura Johnston, Neil R. Aggarwal, Brian T. Garibaldi, V. Sidhaye, Eric Chau, Ronald Cohn, Franco R. D'Alessio, Landon S. King, and Michael T. Crow. "Skeletal Muscle Wasting In Acute Lung Injury Is Suppressed In The Myostatin Null Mouse." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6610.

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Poberezhets, V., A. Demchuk, and Y. Mostovoy. "Compliance to pharmacological therapy of COPD patients with skeletal muscle dysfunction." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.3992.

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Shi, Lingyan, Phyllis Chang, Audrey Zeng, Yajuan Li, and Bryan Bergman. "SRS imaging of lipid-associated mitochondrial dysfunction in human skeletal muscle." In Multiphoton Microscopy in the Biomedical Sciences XXII, edited by Ammasi Periasamy, Peter T. So, and Karsten König. SPIE, 2022. http://dx.doi.org/10.1117/12.2614093.

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Poberezhets, Vitalii, Yuriy Mostovoy, and Anna Demchuk. "COPD patients with skeletal muscle dysfunction VS patients without impairment of skeletal muscle. Comparing features of COPD and life quality." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4309.

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Reports on the topic "Skeletal muscle dysfunction and wasting"

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Jalil, Yorschua, and Ruvistay Gutierrez. Myokines secretion and their role in critically ill patients. A scoping review protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0048.

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Review question / Objective: 1-How and by which means stimulated muscle from critically ill patients can liberate myokines?, 2-Which are the main characteristics of the critically ill population studied and if some of these influenced myokine´s secretion?, 5-Can myokines exert local or distant effects in critically ill patients?, 5-Which are the potential effects of myokines in critically ill patients? Eligibility criteria: Participants and context: We will include primary studies (randomized or non-randomized trials, observational studies, case series or case report) that consider hospitalized critically ill adult patients (18 years or older) in risk for developing some degree of neuromuscular disorders such as ICU-AW, diaphragmatic dysfunction, or muscle weakness, therefore the specific setting will be critical care. Concept: This review will be focused on studies regarding the secretion or measure of myokines or similar (exerkines, cytokines or interleukin) by any mean of muscle activation or muscle contraction such as physical activity, exercise or NMES, among others. The latter strategies must be understood as any mean by which muscle, and there for myocytes, are stimulated as result of muscle contraction, regardless of the frequency, intensity, time of application and muscle to be stimulated (upper limb, lower limb, thoracic or abdominal muscles). We also will consider myokine´s effects, local or systemic, over different tissues in terms of their structure or function, such as myocytes function, skeletal muscle mass and strength, degree of muscle wasting or myopathies, among others.

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