Bibliografie tematiche / Skeletal muscle fibrosis

Letteratura scientifica selezionata sul tema "Skeletal muscle fibrosis"

Autore: Grafiati

Pubblicato: 14 marzo 2023

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Articoli di riviste sul tema "Skeletal muscle fibrosis":

Mahdy, Mohamed A. A. "Skeletal muscle fibrosis: an overview". Cell and Tissue Research 375, n. 3 (12 novembre 2018): 575–88. http://dx.doi.org/10.1007/s00441-018-2955-2.

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Amani, Majid, Masoud Rahmati, Mohammad Fathi e Hasan Ahmadvand. "Reduce Muscle Fibrosis through Exercise via NRG1/ErbB2 Modification in Diabetic Rats". Journal of Diabetes Research 2020 (14 maggio 2020): 1–8. http://dx.doi.org/10.1155/2020/6053161.

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Diabetic myopathy refers to the manifestations in the skeletal muscle as a result of altered glucose homeostasis which reflects as fibrosis. Since physical exercise has been indicated a protective strategy for improving glucose metabolism in skeletal muscle, we tested a hypothesis under which the endurance exercise training could reverse the produced skeletal muscle fibrosis by diabetes. Eight-week-old male Wistar rats were randomly assigned into four groups including healthy control (HC), healthy trained (HT), diabetic control (DC), and diabetic trained (DT) groups. Diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ; 45 mg/kg). Rats in the HT and DT groups carried out an exercise program on a motorized treadmill for five days a week over six weeks. Skeletal muscle levels of NRG1and ErbB2 were measured by the Western blot method. Exercise training decreased blood glucose levels in the DT group. Induction of diabetes increased skeletal muscle fibrosis in both the fast extensor digitorum longus (EDL) and slow soleus muscles, while endurance training modified it in diabetic trained rats. Moreover, muscle NRG1and ErbB2 levels were increased in diabetic rats, while training modified muscle NRG1and ErbB2 levels in diabetic trained rats. Our study provides novel evidence that endurance training could modify skeletal muscle fibrosis through NRG1/ErbB2 modification in STZ-induced diabetic rats.

Meyer, Gretchen A., e Richard L. Lieber. "Skeletal muscle fibrosis develops in response to desmin deletion". American Journal of Physiology-Cell Physiology 302, n. 11 (1 giugno 2012): C1609—C1620. http://dx.doi.org/10.1152/ajpcell.00441.2011.

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Skeletal muscle is a dynamic composite of proteins that responds to both internal and external cues to facilitate muscle adaptation. In cases of disease or altered use, these messages can be distorted resulting in myopathic conditions such as fibrosis. In this work, we describe a mild and progressive fibrotic adaptation in skeletal muscle lacking the cytoskeletal intermediate filament protein desmin. Muscles lacking desmin become progressively stiffer, accumulate increased collagen, and increase expression of genes involved in extracellular matrix turnover. Additionally, in the absence of desmin, skeletal muscle is in an increased state of inflammation and regeneration as indicated by increased centrally nucleated fibers, elevated inflammation and regeneration related gene expression, and increased numbers of inflammatory cells. These data suggest a potential link between increased cellular damage and the development of fibrosis in muscles lacking the cytoskeletal support of the desmin filament network.

Zhao, Na, Bo Liu, Si-Wen Liu, Wei Zhang, Hua-Nan Li, Geng Pang, Xiong-Fei Luo e Jin-Gui Wang. "The Combination of Electroacupuncture and Massage Therapy Alleviates Myofibroblast Transdifferentiation and Extracellular Matrix Production in Blunt Trauma-Induced Skeletal Muscle Fibrosis". Evidence-Based Complementary and Alternative Medicine 2021 (7 luglio 2021): 1–10. http://dx.doi.org/10.1155/2021/5543468.

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Complementary therapies, such as acupuncture and massage, had been previously reported to have therapeutic effects on skeletal muscle contusions. However, the recovery mechanisms on skeletal muscles after blunt trauma via the combination of electroacupuncture (EA) and massage therapy remain unclear. In the present study, a rat model of the skeletal muscle fibrosis following blunt trauma to rat skeletal muscle was established, and the potential molecular mechanisms of EA + massage therapy on the skeletal muscle fibrosis were investigated. The results suggested that EA + massage therapy could significantly decrease inflammatory cells infiltration and collagenous fiber content and ameliorate the disarrangement of sarcomeres within myofibrils compared to the model group. Further analysis revealed that EA + massage therapy could reduce the degree of fibrosis and increase the degree of myofibroblast apoptosis by downregulating the mRNA and protein expression of transforming growth factor- (TGF-) β1 and connective tissue growth factor (CTGF). Furthermore, the fibrosis of injured skeletal muscle was inhibited after treatment through the normalization of balance between matrix metalloproteinase- (MMP-) 1 and tissue inhibitor of matrix metalloproteinase (TIMP). These findings suggested that the combination of electroacupuncture and massage therapy could alleviate the fibrotic process by regulating TGF β1-CTGF-induced myofibroblast transdifferentiation and MMP-1/TIMP-1 balance for extracellular matrix production.

Lieber, Richard L., e Samuel R. Ward. "Cellular Mechanisms of Tissue Fibrosis. 4. Structural and functional consequences of skeletal muscle fibrosis". American Journal of Physiology-Cell Physiology 305, n. 3 (1 agosto 2013): C241—C252. http://dx.doi.org/10.1152/ajpcell.00173.2013.

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Skeletal muscle fibrosis can be a devastating clinical problem that arises from many causes, including primary skeletal muscle tissue diseases, as seen in the muscular dystrophies, or it can be secondary to events that include trauma to muscle or brain injury. The cellular source of activated fibroblasts (myofibroblasts) may include resident fibroblasts, adult muscle stem cells, or inflammatory or perivascular cells, depending on the model studied. Even though it is likely that there is no single source for all myofibroblasts, a common mechanism for the production of fibrosis is via the transforming growth factor-β/phosphorylated Smad3 pathway. This pathway and its downstream targets thus provide loci for antifibrotic therapies, as do methods for blocking the transdifferentiation of progenitors into activated fibroblasts. A structural model for the extracellular collagen network of skeletal muscle is needed so that measurements of collagen content, morphology, and gene expression can be related to mechanical properties. Approaches used to study fibrosis in tissues, such as lung, kidney, and liver, need to be applied to studies of skeletal muscle to identify ways to prevent or even cure the devastating maladies of skeletal muscle.

Moyer, Adam L., e Kathryn R. Wagner. "Regeneration versus fibrosis in skeletal muscle". Current Opinion in Rheumatology 23, n. 6 (novembre 2011): 568–73. http://dx.doi.org/10.1097/bor.0b013e32834bac92.

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Li, Zhao Bo, Helen D. Kollias e Kathryn R. Wagner. "Myostatin Directly Regulates Skeletal Muscle Fibrosis". Journal of Biological Chemistry 283, n. 28 (3 maggio 2008): 19371–78. http://dx.doi.org/10.1074/jbc.m802585200.

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Pidlisetskyy, Andriy, Serhii Savosko, Igor Gayovich, Oleksii Dolhopolov e Volodymyr Biliavskyi. "THE ULTRASONOGRAPHY EXAMINATION OF SKELETAL MUSCLES IN TRAUMATIC ISCHEMIA (EXPERIMENTAL STUDY)". Wiadomości Lekarskie 76, n. 1 (gennaio 2023): 175–81. http://dx.doi.org/10.36740/wlek202301124.

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The aim: To establish indicators and significance of sonography in the evaluation of muscle necrosis in ischemia of the limb acording to quantitative ultrasonographic indicators and density of collagen by histological method. Materials and methods: In experiments, rabbits modeled with 6-hour limb ischemia by applying an elastic tourniquet. On days 5, 15, and 30, ultrasound and histological studies of the muscles and correlation analysis were performed between the muscles’ entropy and the degree of their damage (atrophy, fibrosis and necrosis). Results: The relative amount of structurally altered tissue was estimated morphometrically and compared with entropy. A high correlation of muscle damage with vertical δ-entropy indicates that sonography is highly likely to detect areas of necrosis and, to a lesser extent, fibrosis in the development of ischemic limb contracture in the early stages. Conclusions: Vertical δ-entropy in sonography is a significant indicator of muscle damage after traumatic ischemia and has strong relationship with muscle fibrosis.

Chen, Wan-Jing, I.-Hsuan Lin, Chien-Wei Lee e Yi-Fan Chen. "Aged Skeletal Muscle Retains the Ability to Remodel Extracellular Matrix for Degradation of Collagen Deposition after Muscle Injury". International Journal of Molecular Sciences 22, n. 4 (20 febbraio 2021): 2123. http://dx.doi.org/10.3390/ijms22042123.

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Aging causes a decline in skeletal muscle function, resulting in a progressive loss of muscle mass, quality, and strength. A weak regenerative capacity is one of the critical causes of dysfunctional skeletal muscle in elderly individuals. The extracellular matrix (ECM) maintains the tissue framework structure in skeletal muscle. As shown by previous reports and our data, the gene expression of ECM components decreases with age, but the accumulation of collagen substantially increases in skeletal muscle. We examined the structural changes in ECM in aged skeletal muscle and found restricted ECM degradation. In aged skeletal muscles, several genes that maintain ECM structure, such as transforming growth factor β (TGF-β), tissue inhibitors of metalloproteinases (TIMPs), matrix metalloproteinases (MMPs), and cathepsins, were downregulated. Muscle injury can induce muscle repair and regeneration in young and adult skeletal muscles. Surprisingly, muscle injury could not only efficiently induce regeneration in aged skeletal muscle, but it could also activate ECM remodeling and the clearance of ECM deposition. These results will help elucidate the mechanisms of muscle fibrosis with age and develop innovative antifibrotic therapies to decrease excessive collagen deposition in aged muscle.

Tonogai, Ichiro, e Ichiro Tonogai. "Influence of Platelet Rich Plasma on the Skeletal Muscle Fibrosis after Limb Lengthening in Mice". Foot & Ankle Orthopaedics 5, n. 4 (1 ottobre 2020): 2473011420S0046. http://dx.doi.org/10.1177/2473011420s00468.

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Category: Basic Sciences/Biologics Introduction/Purpose: Skeletal muscle fibrosis induced by the increase of collagen occurs after limb lengthening which is also called distraction osteogenesis. Although there are studies about influence of platelet rich plasma (PRP) on tissues healing process, its effectiveness is still controversial. The aim of this study was to examine whether PRP decreased the skeletal muscle fibrosis induced by limb lengthening. Methods: Tibial osteotomy was done to 8-week-old wild type mice. Tibia was lengthened at a rate of 0.42 mm/day during 2 weeks, launching 1 week after tibial osteotomy. Just after lengthening completed (3 weeks after tibial osteotomy), PRP was injected into the gastrocnemius muscle (PRP group). As a sham group, phosphate buffered saline (PBS) was injected into the gastrocnemius muscle (non-PRP group). The gastrocnemius (GC) muscles were taken and analyzed at 4, 6, 8 and 10 weeks after tibial osteotomy. Results: The fibrotic area of the GC muscles in the both groups increased at 4 weeks after tibial osteotomy in histological analysis (Figure). Then, it gradually decreased at 6, 8, and 10 weeks after tibial osteotomy. There were no significant differences between the both groups at 6, 8, and 10 weeks after tibial osteotomy. Hydroxyproline, which was a major constituent of collagen, increased in the non-PRP and PRP groups by limb lengthening as well. However, significant changes were not found between the both groups at all any points. Conclusion: At first, we anticipated that PRP should reduce the skeletal muscle fibrosis after limb lengthening significantly. But our results implied that PRP did not decrease the skeletal muscle fibrosis induced by limb lengthening.

Più fonti

Tesi sul tema "Skeletal muscle fibrosis":

Smith, Cheryl A. "Skeletal muscle injury, fibrosis and transforming growth factor-[beta]". Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1744.

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Thesis (Ph. D.)--West Virginia University, 2000.
Title from document title page. Document formatted into pages; contains xii, 146 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

van, Erp Christel. "Modifying function and fibrosis of cardiac and skeletal muscle from mdx mice". University of Southern Queensland, Faculty of Sciences, 2005. http://eprints.usq.edu.au/archive/00001521/.

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Duchenne Muscular Dystrophy (DMD) is a fatal condition occurring in approximately 1 in 3500 male births and is due to the lack of a protein called dystrophin. Initially DMD was considered a skeletal myopathy, but the pathology and consequences of cardiomyopathy are being increasingly recognised. Fibrosis, resulting from continual cycles of degeneration of the muscle tissues followed by inadequate regeneration of the muscles, is progressive in both cardiac and skeletal dystrophic muscle. In the heart fibrosis interferes with contractility and rhythm whereas it affects contractile function and causes contractures in skeletal muscles. This study utilised the mdx mouse which exhibits a pathological loss of muscle fibres and fibrosis characteristic of DMD, to examine a range of mechanisms that can influence muscle function and fibrosis. Ageing and workload both appear to contribute to the development of dystrophic features in cardiac and skeletal muscle of the mdx mouse. Therefore the effect of eccentric exercise on cardiac and skeletal muscle was examined in older mdx mice. Mice ran in 30 minute sessions for five months, 5 days per week. Downhill treadmill running did not exacerbate the contractile function or fibrosis of the mdx heart or the EDL, SOL or diaphragm muscles suggesting that cytokines influence function and fibrosis to a greater extent than workload alone. The role of the cytokine TGF-beta was examined by treating mdx mice with the TGF-beta antagonist pirfenidone at 0.4, 0.8 or 1.2 per cent in drinking water for six months. Pirfenidone improved cardiac contractility (P<0.01) and coronary flow (P<0.05), to levels comparable to control mice, despite no reduction in cardiac fibrosis. Pirfenidone did not reduce fibrosis or improve function in skeletal muscle. A deficiency of neuronal nitric oxide synthase (nNOS) in DMD and mdx mice causes a lowered production of nitric oxide indicating that the substrate of nNOS, l-arginine, may be beneficial to cardiac and skeletal muscle function in mdx mice. Oral l-arginine (5 mg/g bw) improved cardiac contractility, coronary flow and reduced cardiac fibrosis (P<0.05) without improving skeletal muscle function or fibrosis. In contrast, 10 mg/g bw l-arginine improved cardiac function and coronary flow (P<0.01), despite also elevating cardiac collagen. This increment in collagen was prevented by co-administration of prednisone. The experiments described in this dissertation reveal for the first time that pharmacological treatments in mdx mice can improve cardiac structure and function. Further elucidation of the optimum time and doses of such treatments may result in future pharmacological treatments to improve cardiac function and fibrosis in DMD.

Puliti, Elisa. "Role of sphingosine 1-phosphate metabolism and signalling in skeletal muscle atrophy and fibrosis". Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1195603.

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In the last 30 years, multiple roles of S1P have been demonstrated in the regulation of skeletal muscle biology. The presented study is focused on the role of S1P metabolism in myogenic differentiation, where SPL was found playing a crucial role in regulating S1P cellular levels and responsible for onset of myogenic program. The role of S1P axis was also confirmed in skeletal muscle atrophy induced by TNF-alpha. S1P signalling pathwayplays a crucial role in the development and maintenance of the fibrotic process. New S1P3 antagonists were tested to antagonise the receptor involved in fibrosis, and new SK inhibitors have been designed on the base of PF-543, with the aim to develop glycohybrids as potential pharmacological tool in skeletal muscle fibrosis. The metabolism of S1P appears a promising drug targets for pharmacological therapies in skeletal muscle repair.

Cai, Weisong, e 蔡蔚松. "Cystic fibrosis transmembrane conductance regulator is involved in therelease of ATP from contracting skeletal muscle". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49618088.

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Contracting skeletal muscle releases ATP into the interstitial space where it is subsequently broken down to adenosine by the action of ecto-5’-nucleotidase. Both ATP and adenosine are vasodilators that contribute to the exercise hyperaemia. However, the mechanism for the release of ATP from muscle during exercise remains unknown. Cystic fibrosis transmembrane conductance regulator (CFTR) is involved in ATP release from muscle at low intracellular pH: this study was performed to investigate whether CFTR was involved in the ATP release from skeletal muscle during contractions. Experiments were performed in rats anaesthetised with sodium pentobarbitone and breathing spontaneously. A microdialysis probe was placed in one gastrocnemius muscle: ATP was determined in interstitial microdialysate samples using a bioluminescence assay. The sciatic nerve was stimulated to induce two bouts of muscle contractions, separated by a recovery period of 40 mins; one of the inhibitors was administered prior to the second bout of contractions. Muscle contractions elevated the interstitial ATP by 1500 to 3000%. In the control experiments, no drug was given: both the contractile force and the increase in interstitial ATP were reproducible in repeated contraction bouts. Infusion of a specific inhibitor of CFTR, CFTRinh-172, did not alter the contractile force, but significantly lowered the interstitial ATP during muscle contractions, suggesting that CFTR was involved in the contraction-induced ATP release. Similarly, infusion of the Protein Kinase A inhibitor, KT5720, significantly reduced interstitial ATP during muscle contractions without altering contractile force, suggesting that CFTR in skeletal muscle is activated through the cAMP/PKA pathway. The increase in interstitial ATP during muscle contraction was also inhibited by the Na/H exchanger inhibitor, amiloride, or the Na/Ca exchanger inhibitor, SN6. It has been also shown that two gap junction hemichannel inhibitors, gadolinium and carbenoxolone, could attenuate the increase of ATP during muscle contraction. These data suggest that CFTR, activated through the cAMP/protein kinase A pathway, is involved in the ATP release during muscle contraction, and that activation of the Na/H exchanger and Na/Ca exchanger was also required, indicating that the signal transduction mechanism for CFTR activation during muscle contractions may be similar to that which is reported to occur at low pH. The preliminary data showed that the gap junction hemichannels might mediate the ATP release from skeletal muscle cells during muscle contraction.
published_or_final_version
Physiology
Master
Master of Philosophy

Lu, Lin, e 鹿琳. "The involvement of connexin hemichannels and cystic fibrosis transmembrane conductance regulator in acidosis-induced ATP release from skeletal myocytes". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208017.

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The cystic fibrosis transmembrane conductance regulator (CFTR) was identified to be involved in acidosis-induced ATP release from skeletal myocytes in vitro and from contracting muscle in vivo. My PhD studies aimed to investigate the underlying mechanism and identify the pathway for ATP release in acidosis-induced CFTR-regulated ATP release. Lactic acid (10 mM) decreased the intracellular pH of L6 skeletal myocytes to 6.87 ± 0.12 after 3 hours, and the lowered pH resulted in the elevation of ATP release from skeletal myocytes. The acidosis-induced ATP release was totally abolished by GlyH-101 (40 μM), an open-channel CFTR blocker, suggesting that CFTR was involved. The cAMP/PKA signaling pathway was involved in the CFTR-regulated ATP release from skeletal myocytes: 1). Forskolin increased the extracellular ATP and the phosphorylation of CFTR; IBMX, a phosphodiesterase inhibitor, further enhanced the forskolin-induced extracellular ATP and phosphorylation of CFTR; 2). Inhibition of PKA by its selective inhibitor KT-5720 abolished the acidosis-induced ATP release and the forskolin-induced phosphorylation of CFTR. In addition, the inhibition of Na+/H+ exchanger (NHE) by amiloride, or inhibition of Na+/Ca2+ exchanger (NCX) by its specific inhibitors SN-6 and KB-R7943 abolished the lactic-acid-induced ATP release from skeletal myocytes, indicating that NHE and NCX might be involved. Previous studies demonstrated that Connexin hemichannels and Pannexin channels were able to conduct ATP in response to stimuli. This study found that connexin 43 (Cx43) was strongly expressed on skeletal myocytes, while Pannexin 1 (Panx1) showed a strong expression in gastrocnemius muscle. Investigation of the role that Cx43 may play in acidosis-induced cAMP/PKA-activated CFTR-regulated ATP release from myocytes showed that: 1). Cx43 was immunoprecipitated with CFTR suggesting a physical interaction; 2). The opening of Cx hemichannels was increased by lactic acid and this lactic-acid-induced opening was inhibited by CFTRinh-172, suggesting the mediation of CFTR; 3). Inhibition of Cxs and Panxs with carbenoxolone abolished the acidosis-induced ATP release; moreover, specific silencing of the Cx43 gene using siRNA decreased both basal and acidosis-induced ATP release, suggesting that Cx43 was involved; 4). Overexpression of CFTR alone did not elevate the acidosis-induced ATP release, while overexpression of Cx43 alone doubled the acidosis-induced ATP, and co-overexpression of CFTR and Cx43 further elevated the acidosis-induced ATP release, supporting the concept that Cx43 functionally interacted with CFTR to induce the acidosis-induced ATP release. Panx1 was studied in native skeletal muscle, and found to be coimmunoprecipitated with CFTR. Inhibition of Panxs with gadolinium or probenecid abolished the muscle-contraction-induced ATP release, while inhibition with carbenoxolone or quinine reduced it to less than 10% of control, suggesting that Panx1 may be involved in the acidosis-induced ATP release during muscle contraction. All the in vitro and in vivo studies suggested that Cxs and Panx were involved in the acidosis-induced CFTR-regulated ATP release from skeletal myocytes and skeletal muscle.
published_or_final_version
Physiology
Doctoral
Doctor of Philosophy

Pinto, Priscilla Avelino Ferreira. "Treino de baixa intensidade retarda a deposi??o de fibras col?genas no m?sculo gastrocn?mio distr?fico de modelo mdx". UFVJM, 2017. http://acervo.ufvjm.edu.br/jspui/handle/1/1608.

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Funda??o de Amparo ? Pesquisa do Estado de Minas Gerais (FAPEMIG)
Introdu??o: A Distrofia Muscular de Duchenne (DMD) ? marcada pela falta da distrofina, e sua aus?ncia leva a altera??es mec?nicas da fibra muscular, resultando num processo de necrose muscular e altera??es histol?gicas. O treinamento f?sico de baixa intensidade vem sendo empregado como forma de retardar a progress?o da DMD, entretanto, ainda n?o se sabe os par?metros ben?ficos ao m?sculo distr?fico. Assim, objetivou-se elucidar os efeitos do exerc?cio terap?utico de baixa intensidade em esteira no m?sculo esquel?tico distr?fico do modelo mdx nos par?metros morfol?gicos, na morfometria dos marcadores de les?o muscular, da fibrose musclar e na constitui??o da matriz extracelular pelos col?genos tipo I e III. Metodologia: Foram estudados tr?s grupos: camundongos mdx exerc?cio (mdxE), mdx sedent?rio (mdxC) e controle saud?veis (Cc) (n=8/grupo). O grupo mdxE foi estimulado a correr em esteira horizontal motorizada para ratos, em baixa intensidade, 9m/min por 30 minutos/dia, 3 vezes/semana, por 8 semanas. Ap?s o protocolo de exerc?cio foi realizada a eutan?sia dos animais e coletado o m?sculo gastrocn?mio. Foi realizada a colora??o Hematoxilina-Eosina para an?lise dos marcadores de les?o muscular: N?cleo Central e Di?metro M?nimo de Feret; a rea??o de Picrossirius red para an?lise das fibras col?genas na fibrose muscular e a imuno-localiza??o das fibras col?genas tipo I e III. Resultados: Foram observadas altera??es histol?gicas distr?ficas caracter?sticas nos grupos mdxE e mdxC e feixes de fibras col?genas espessas no grupo mdxC. A imuno-histoqu?mica revelou presen?a de col?geno do tipo I principalmente no grupo mdxC. N?o houve diferen?a significativa entre os grupos mdxE e mdxC para fibras com n?cleo central e coeficiente de varia??o do Di?metro m?nimo de Feret. O grupo mdxE n?o apresentou diferen?a significativa em rela??o ao Cc para a porcentagem da ?rea de fibras col?genas na fibrose muscular. Conclus?es: O treino de baixa intensidade reduz a deposi??o de fibras col?genas na fibrose muscular, com fibras delgadas do col?geno tipo I e n?o altera os marcadores de les?o muscular.
Disserta??o (Mestrado Profissional) ? Programa de P?s-Gradua??o em Reabilita??o e Desempenho Funcional, Universidade Federal dos Vales do Jequitinhonha e Mucuri, 2017.
Introduction: Duchenne muscular dystrophy (DMD) is marked by lack of dystrophin, and its absence leads to muscle fiber rupture, resulting in muscular necrosis and histological changes. Physical training of low intensity has been used to delay the progression of DMD, however, parameters of the dystrophic muscle are not yet known. The objective of this study was to elucidate the effects of a treadmill low intensity exercise on morphology, morphometric parameters of the muscle injury markers and the composition of the extracellular matrix by type I and III collagens of the dystrophic skeletal muscle of the mdx model. Methods: Three groups were studied: exercised mdx (mdxE), sedentary mdx (mdxC) and healthy controls (Cc) (n =8/group). The mdxE group was stimulated to run on a motorized horizontal treadmill for rats, with a low intensity (9 m/min for 30 minutes/day, 3 times/week) for 8 weeks. After the exercise protocol, the animals were euthanized and the gastrocnemius muscle was collected. Hematoxylin-Eosin staining was performed for analysis of muscle injury markers, Central Nucleus and Minimum Diameter of Feret, Picrossirius red reaction for analysis of collagen fibers in muscle fibrosis and immuno-localization of type I and III collagen fibers. Results: Dystrophic histopathological changes were observed in the mdxE and mdxC groups and thicker collagen fiber bundles in the mdxC group. Immunohistochemistry revealed the presence of type I collagen mainly in the mdxC group. There was no significant difference between the mdxE and mdxC groups for fibers with centrally located nuclei and coefficient of variation of the Minimum Feret Diameter. The mdxE group showed no significant difference in relation to Cc for the percentage of the area of collagen fibers in muscle fibrosis. Conclusions: The low intensity training reduced the deposition of collagen fibers in muscle fibrosis with thin fibers of type I collagen and did not alter the markers of muscle injury.

Hauck, James Spencer. "Mineralocorticoid Receptor Signaling in Acute and Chronic Muscle Injury". The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1565089935933727.

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Neves, Juliana de Carvalho. "Envolvimento da neuraminidase-1 na regeneração muscular". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-06052014-091743/.

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A neuraminidase-1 (Neu1) participa da regulação do catabolismo de sialoglicoconjugados nos lisossomos. A deficiência congênita da Neu1 é a base da sialidose, doença neurossomática grave associada a deformidades osteoesqueléticas, hipotonia e fraqueza muscular. Camundongos com deficiência de Neu1 (Neu1-/-) desenvolvem uma forma atípica de degeneração muscular caracterizada por expansão da matriz extracelular (MEC), invasão das fibras musculares por fibroblastos, fragmentação do citoplasma, formação vacuolar e atrofia muscular. Apesar de a degeneração muscular estar bem caracterizada nestes animais, a miogênese ainda não havia sido estudada. O objetivo desta pesquisa foi avaliar o envolvimento da Neu1 no processo de regeneração muscular, após aplicação de cardiotoxina (CTX) em camundongos Neu1-/-, em comparação com controles normais. A CTX foi administrada no músculo tibial anterior direito e os animais foram eutanasiados por deslocamento cervical 1, 3, 5, 7, 10, 14, 21 e 28 dias após a lesão. Os músculos foram analisados através de histologia; medição da área transversa das fibras musculares centronucleadas; verificação do potencial proliferativo celular por quantificação de marcação de BrdU; imunoistoquímica para inflamação, fibras regenerativas e fibrose; e expressão gênica e proteica de fatores de transcrição musculares. Os dados foram comparados estatisticamente e as variações significativas devem apresentar p <= 0,05. Nos animais com deficiência de Neu1, o processo inflamatório (especialmente a reação macrofágica) e o potencial proliferativo estavam aumentados nas fases iniciais, acompanhados da hiperexpressão de Pax7. Observamos atraso na maturação muscular caracterizado por maior expressão de miosina embrionária em estágios mais tardios da regeneração. Os genes MyoD e MyoG estavam com expressão aumentada no período de 5 a 10 dia após a lesão, embora a expressão destas proteínas estivesse reduzida. Ao final da regeneração, houve maior deposição de reticulina na MEC, indicando processo fibrótico. A Neu1 parece atuar em todos os estágios da regeneração muscular, desde a fase aguda da lesão através do controle da proliferação celular, até a maturação muscular e estágios finais em que regularia a deposição de componentes da MEC
Neuraminidase-1 (Neu1) participates in sialoglycoconjugates catabolism in lysosomes. Congenital Neu1 deficiency is the basis of sialidosis, a severe neurosomatic disorder associated with osteoskeletal deformities, hypotonia and muscle weakness. Mice with Neu1 deficiency (Neu1-/-) develop an atypical form of muscle degeneration characterized by abnormal fibroblast proliferation and expanded extracellular matrix (ECM), invasion of muscle fibers by fibroblast, cytosolic fragmentation, vacuolar formation and muscle atrophy. Despite muscle degeneration is well characterized in these animals, myogenesis has not been studied so far. The aim of this study was to evaluate the involvement of Neu1 in muscle regeneration process after cardiotoxin (CTX) injection in Neu1-/- mice and normal controls. CTX was applied in the right tibialis anterior muscle, and the animals were euthanized by cervical dislocation 1, 3, 5, 7, 10, 14, 21 and 28 days after injury. The muscles were analyzed through histology; cross-sectional area of regenerative muscle fibers; quantification of BrdU labeling; immunohistochemistry labelling for inflammation, regenerative fibers, and fibrosis; and gene and protein expression of muscle transcription factors. The data were compared and variances considered statistically significant in case p <= 0.05. In animals with Neu1 deficiency, both inflammatory process (mainly macrophagic response) and proliferative potential were increased in the initial stages, accompanied by overexpression of Pax7. We observed delay in muscle maturation characterized by higher expression of embryonic myosin later in muscle regeneration. MyoD and MyoG genes were overexpressed from 5 to 10 days after injury, though the expression of these proteins was reduced. At the end of muscle regeneration, reticulin deposition in ECM was increased, indicating fibrotic process. Neu1 seems to participate in all stages of muscle regeneration, since acute injury phase through the control of cell proliferation, towards muscle maturation, and at the final stages when it would regulate the deposition of ECM components

Ranasinghesagara, Janaka C. Yao Gang. "Optical reflectance in fibrous tissues and skeletal muscles". Diss., Columbia, Mo. : University of Missouri--Columbia, 2008. http://hdl.handle.net/10355/6629.

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Title from PDF of title page (University of Missouri--Columbia, viewed on March 8, 2010). The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Dissertation advisor: Dr. Gang Yao. Vita. Includes bibliographical references.

Huber, Adrian Thomas. "Multi-organ non-invasive tissue characterization of fibrosis, adipose tissue, edema and inflammation with magnetic resonance (MR) imaging : applications to myocardium, skeletal muscle and liver interactions Cardiac MR strain: a noninvasive biomarker of fibro-fatty remodeling of the left atrial myocardium Comparison of MR T1 and T2 mapping parameters to characterize myocardial and skeletal muscle involvement in systemic Idiopathic Inflammatory Myopathy (IIM) Non-invasive differentiation of acute viral myocarditis and idiopathic inflammatory myopathy with cardiac involvement using magnetic resonance imaging T1 and T2 mapping CT predicts liver fibrosis: Prospective evaluation of morphology- and attenuationbased quantitative scores in routine portal venous abdominal scans". Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS135.

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Cette thèse réalise une preuve de concept pour quantifier la déformation de l’oreillette gauche (OG) en IRM, ainsi que la relaxométrie IRM dans le myocarde, dans les muscles squelettiques et dans le foie. Grâce à l’interaction entre radiologues et ingénieurs, deux logiciels différents ont été développés, appliqués et validés pour l'analyse de la déformation myocardique multi-chambre et pour la cartographie quantitative du T1 multi-organes. La première publication a montré une forte corrélation de la déformation de l’OG, avec le degré de remplacement fibro-graisseux en histologie. Ce biomarqueur d'imagerie fonctionnelle est prometteur, puisque le remodelage structurel du myocarde est un substrat morphologique connu du dysfonctionnement électro-physiologique et de la fibrillation atriale. La deuxième publication a démontré l'influence de la composition et de la vascularisation de différents tissus sur les paramètres cartographiques T1. ΔT1 (prise de contraste musculaire relative) et EHF (prise de contraste musculaire normalisée par la prise de contraste dans le sang) ont été introduits comme alternatives simples au volume extracellulaire (ECV). Dans la troisième publication, les paramètres de relaxométrie appliqués aux muscles squelettiques ont permis une discrimination entre patients avec myocardite aiguë et patients avec des myosites systémiques. La quatrième publication a introduit le T1 du foie pour quantifier l’insuffisance cardiaque chez des patients avec des cardiomyopathies idiopathiques dilatées, montrant de meilleures performances que les paramètres fonctionnels établis tels que les volumes, la fraction d'éjection ou la déformation myocardique
This thesis provides a proof of concept for MR atrial strain, as well as MR relaxometry in the myocardium, in skeletal muscles and in the liver. Thanks to a close interaction between radiologist and software engineers, two different softwares were developed, applied and validated: one for multiorgan T1 mapping in the myocardium, skeletal muscle and liver, another one for cardiac four-chamber strain analysis and volumetry. The first publication showed a strong correlation of LA strain with the degree of fibro-fatty replacement in histology. Such functional imaging biomarker in combination with LA volumetry could help to guide clinical decisions, since myocardial structural remodeling is a known morphologic substrate of LA dysfunction, atrial fibrillation and adverse outcome. In the second publication, MR relaxometry parameters applied to the myocardium and skeletal muscles in IIM patients and healthy volunteers were used as a model to demonstrate influences of different tissue composition and vascularization on T1 mapping parameters. ΔT1 and EHF were introduced as simple alternatives to ECV in highly vascularized tissues such as the myocardium. In the third publication, MR relaxometry parameters applied to the skeletal muscls allowed for an accurate discrimination of AVM and IIM with cardiac involvement. However, when applied to the myocardium, parametric mapping did not separate between the two groups. The fourth publication introduced native T1 of the liver an easily accessible and accurate non-invasive imaging associate of congestive HF in IDCM patients with better performance than established functional parameters such as LV volumes, ejection fraction or strain

Capitoli di libri sul tema "Skeletal muscle fibrosis":

Pessina, Patrizia, e Pura Muñoz-Cánoves. "Fibrosis-Inducing Strategies in Regenerating Dystrophic and Normal Skeletal Muscle". In Methods in Molecular Biology, 73–82. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3810-0_7.

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Elhussieny, Ahmed, Ken’ichiro Nogami, Fusako Sakai-Takemura, Yusuke Maruyama, AbdElraouf Omar Abdelbakey, Wael Abou El-kheir, Shin’ichi Takeda e Yuko Miyagoe-Suzuki. "Mesenchymal Stem Cells for Regenerative Medicine for Duchenne Muscular Dystrophy". In Muscular Dystrophy - Research Updates and Therapeutic Strategies. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.92824.

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Mesenchymal stem cells (MSCs) are multipotent stem cells that can be isolated from both foetal and adult tissues. Several groups demonstrated that transplantation of MSCs promoted the regeneration of skeletal muscle and ameliorated muscular dystrophy in animal models. Mesenchymal stem cells in skeletal muscle, also known as fibro-adipogenic progenitors (FAPs), are essential for the maintenance of skeletal muscle. Importantly, they contribute to fibrosis and fat accumulation in dystrophic muscle. Therefore, MSCs in muscle are a pharmacological target for the treatment of muscular dystrophies. In this chapter, we briefly update the knowledge on mesenchymal stem/progenitor cells and discuss their therapeutic potential as a regenerative medicine treatment of Duchenne muscular dystrophy.

Lambrechts, Mark. "Musculoskeletal Abnormalities Caused by Cystic Fibrosis". In Advances in Skeletal Muscle Health and Disease [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104591.

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Cystic Fibrosis (CF) can affect all organs of the human body including the musculoskeletal system. Although the musculoskeletal aspects of CF are less commonly studied, fractures (predominantly spinal), muscle injuries, and joint pain are more commonly seen in the CF population compared to the general public due to their lower bone mineral density, dysfunctional skeletal muscle, and elevated levels of pro-inflammatory cytokines. Additionally, due to elevated levels of inflammation in the CF population diagnosis of musculoskeletal injuries can be difficult to pinpoint. As treatment for CF evolves, an increased understanding of how CF affects the musculoskeletal system is imperative. We will discuss the orthopedic aspects of CF and provide potential insights into the future direction of orthopedic care in the CF population.

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Serrano, Antonio L., Christopher J. Mann, Berta Vidal, Esther Ardite, Eusebio Perdiguero e Pura Muñoz-Cánoves. "Cellular and Molecular Mechanisms Regulating Fibrosis in Skeletal Muscle Repair and Disease". In Current Topics in Developmental Biology, 167–201. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-12-385940-2.00007-3.

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Bundgaard, Henning, Anna Axelsson, Alex Christensen e Helle Petri. "The heart in neuromuscular disease: myotonic dystrophy". In ESC CardioMed, 1530–34. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0370.

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Myotonic dystrophy type 1 (DM1) is a multisystemic disease, mainly involving skeletal muscles, the central nervous system, the gastrointestinal tract, and the heart. DM1 is inherited as an autosomal dominant trait. Patients with DM1 have a reduced life expectancy with a mean age at death of approximately 53 years. Fibrosis, fat infiltration, and degeneration are seen in both skeletal muscles and in the myocardium. Cardiac involvement in DM1 patients is a major concern as the cause of death is of cardiac origin in 30% of patients. The major cardiac manifestations, including conduction abnormalities, supraventricular and ventricular arrhythmias, and reduced left ventricular systolic function, may lead to sudden cardiac death (SCD) or death from progressive heart failure. The increased risk of SCD underscores the need for assessment of cardiac involvement in order to prevent SCD. Clinical evaluation at the time of diagnosis and life-long repeated follow-up should include clinical assessment, electrocardiogram, Holter monitoring, and echocardiography. Generally, cardiac manifestations in DM1 patients should be treated according to general guidelines. An important topic to be resolved is whether a subset of patients, not fulfilling traditional criteria for pacemaker implantation, but who are estimated to be at high risk of severe conduction abnormalities, benefit from pacemaker or defibrillator implantation on a primary prophylactic basis.

Atkinson, Martin E. "Introduction and surface anatomy". In Anatomy for Dental Students. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780199234462.003.0029.

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The head and neck contain the structures that are the most significant to the practice of dental surgery. These regions are not as easy to study from dissection as other areas because an ‘onion skin’ approach has to be adopted. Layers are dissected from the most superficial subcutaneous structures to the deepest internal structures, the brain, and spinal cord; structures that appear at one level may not show up again until the dissection has advanced to much deeper layers. It is important to have a general understanding of the structures forming the head and neck to build up a coherent picture of their relationship to each other. The skull is the structural basis of the head. The skull comprises the cranium, formed from 27 bones joined together by fibrous joints known as sutures, and the separate mandible that articulates with the cranium at the temporomandibular joints (TMJ). The skull houses and protects the brain in the cranial cavity. It also protects other delicate structures vital for the reception of the special senses; the orbital cavities contain the eyes and dense bones in the cranial base house the internal ears. The entrance to the respiratory tract is the bony and cartilaginous nasal cavity; it can also be accessed together with the gastrointestinal tract through the oral cavity between the cranium and mandible. The major skeletal component of the neck is the cervical part of the vertebral column formed by seven vertebrae. The lower five cervical vertebrae conform to the general pattern of vertebrae outlined in Section 10.1.1, but the upper two cervical vertebrae are specialized; the atlas articulates with the underside of the skull for nodding movements and the second vertebra, the axis, articulates with the atlas for shaking movements of the head. The hyoid bone in the upper anterior neck and the laryngeal cartilages below it form the laryngeal skeleton. There are several important muscle groups in the head. The muscles of facial expression are small superficial muscles beneath the skin of the face; they alter facial expression in response to emotion, but also play a part in chewing, swallowing, and speech.

Shpadaruk, Volha, e Karen E. Harman. "Cutaneous vasculitis, connective tissue diseases, and urticaria". In Oxford Textbook of Medicine, a cura di Roderick J. Hay, 5639–76. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0556.

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Vasculitis (angiitis) denotes necrotizing inflammation of the blood vessels; occlusive vasculopathy implies vascular occlusion without significant vascular inflammation. A small-vessel cutaneous vasculitis is the most common vasculitis affecting the skin, and may be the first sign of a systemic vasculitis, but 50% of patients have no systemic disease. Systemic lupus erythematosus is diagnosed if four or more of the American College of Rheumatology revised criteria for the classification of this disease are present, either sequentially or simultaneously. Meanwhile, dermatomyositis is an uncommon multisystem autoimmune disease in which inflammatory skin changes are associated with polymyositis of skeletal muscle. Scleroderma means thickened, fibrotic, bound-down skin. It might develop in association with a systemic connective tissue disease (systemic sclerosis) or present as a localized cutaneous problem. Panniculitis is inflammation of the subcutaneous fat, sometimes associated with vasculitis. It presents with erythematous subcutaneous nodules, most often on the lower leg.

Atti di convegni sul tema "Skeletal muscle fibrosis":

Rozenberg, D., M. Sussman, R. G. L. Koh, S. Nourouzpour, L. Wickerson, L. G. Singer, S. Shapera et al. "Skeletal Muscle Size and Fat Infiltration of the Limb Muscles in Idiopathic Pulmonary Fibrosis". In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3179.

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Balañá, Ana, Juana Martínez-Llorens, Diego Agustin Rodríguez, Mireia Admetlló, Anna Salazar, Pilar Ausin, Esther Barreiro e Joaquin Gea. "Skeletal muscle function and structure in patients with non-cystic fibrosis bronchiectasis". In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa265.

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Verges, Samuel, Nicolas Decorte, Mathieu Gruet, Boubou Camara, Sébastien Quetant, Laurent Mely, Jean-Marc Vallier e Bernard Wuyam. "Skeletal muscle metabolism in active cystic fibrosis (CF) patients with light/moderate pulmonary dysfunction". In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2242.

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Wang, Xuejie, Ana Balañá Corberó, Juana Martínez Llorens, Liyun Qin, Mireia Admetlló, Esmeralda Hernández Leal, Xavier Duran, Antonio Sancho Muñoz e Esther Barreiro Portela. "Skeletal Muscle Dysfunction and Body Composition Alterations in Non-Cystic Fibrosis Bronchiectasis Patients: Gender Differences". In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1836.

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Huang, Alice H., Spencer S. Watson e Ronen Schweitzer. "Lineage Tracing Reveals a New Model for Tendon Growth and Elongation During Development". In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80915.

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Tendons are dense, fibrous tissues connecting muscle to bone, and their primary function is to transmit muscle forces to the appropriate skeletal elements, thereby enabling movement. In the limb, flexion and extension of the hand (autopod) and wrist are controlled by long tendons that insert into muscles in the arm (zeugopod) [1]. Although tendons are critically important in mediating joint movement, the cellular and molecular events underlying tendon formation remain largely unknown. Using the transcription factor Scleraxis (Scx), which labels all tendon progenitors, we previously showed that in the mouse limb bud, Scx-expressing tendon progenitors are first induced in the mesenchyme underneath the ectoderm at E10.5; at E12.5, progenitors are loosely organized between the cartilage condensations and developing muscles, condensing to form distinct tendons by E13.5 [2]. By E14.5, limb tendon patterning is largely complete, with continued elongation and deposition of matrix from this stage onward.

Uslu, Nazlı Zeynep, Derya Kocakaya, Sehnaz Olgun Yıldızeli, Emel Eryüksel, Özge Keniş Coşkun, Canan Cimşit, Şeyma Görçin Karaketir e Berrin Ceyhan. "Does cystic fibrosis impact skeletal muscles and diaphragm function?" In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa343.

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Marillier, Mathieu, Anne-Catherine Bernard, Onofre Moran-Mendoza, Denis E. O'Donnell, Samuel Verges e J. Alberto Neder. "Beyond the lungs in fibrotic interstitial lung disease: does supplemental O2 improve skeletal muscle oxygenation and fatigue?" In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.4405.

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