Journal articles: 'Skeletal muscle fibrosis'

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Mahdy, Mohamed A. A. "Skeletal muscle fibrosis: an overview." Cell and Tissue Research 375, no. 3 (November 12, 2018): 575–88. http://dx.doi.org/10.1007/s00441-018-2955-2.

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Amani, Majid, Masoud Rahmati, Mohammad Fathi, and Hasan Ahmadvand. "Reduce Muscle Fibrosis through Exercise via NRG1/ErbB2 Modification in Diabetic Rats." Journal of Diabetes Research 2020 (May 14, 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.

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Meyer, Gretchen A., and Richard L. Lieber. "Skeletal muscle fibrosis develops in response to desmin deletion." American Journal of Physiology-Cell Physiology 302, no. 11 (June 1, 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.

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Zhao, Na, Bo Liu, Si-Wen Liu, Wei Zhang, Hua-Nan Li, Geng Pang, Xiong-Fei Luo, and 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 (July 7, 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.

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Lieber, Richard L., and Samuel R. Ward. "Cellular Mechanisms of Tissue Fibrosis. 4. Structural and functional consequences of skeletal muscle fibrosis." American Journal of Physiology-Cell Physiology 305, no. 3 (August 1, 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.

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Moyer, Adam L., and Kathryn R. Wagner. "Regeneration versus fibrosis in skeletal muscle." Current Opinion in Rheumatology 23, no. 6 (November 2011): 568–73. http://dx.doi.org/10.1097/bor.0b013e32834bac92.

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Li, Zhao Bo, Helen D. Kollias, and Kathryn R. Wagner. "Myostatin Directly Regulates Skeletal Muscle Fibrosis." Journal of Biological Chemistry 283, no. 28 (May 3, 2008): 19371–78. http://dx.doi.org/10.1074/jbc.m802585200.

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Pidlisetskyy, Andriy, Serhii Savosko, Igor Gayovich, Oleksii Dolhopolov, and Volodymyr Biliavskyi. "THE ULTRASONOGRAPHY EXAMINATION OF SKELETAL MUSCLES IN TRAUMATIC ISCHEMIA (EXPERIMENTAL STUDY)." Wiadomości Lekarskie 76, no. 1 (January 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.

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Chen, Wan-Jing, I.-Hsuan Lin, Chien-Wei Lee, and 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, no. 4 (February 20, 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.

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Tonogai, Ichiro, and Ichiro Tonogai. "Influence of Platelet Rich Plasma on the Skeletal Muscle Fibrosis after Limb Lengthening in Mice." Foot & Ankle Orthopaedics 5, no. 4 (October 1, 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.

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Gallardo, Felipe S., Adriana Córdova-Casanova, and Enrique Brandan. "The linkage between inflammation and fibrosis in muscular dystrophies: The axis autotaxin–lysophosphatidic acid as a new therapeutic target?" Journal of Cell Communication and Signaling 15, no. 3 (March 10, 2021): 317–34. http://dx.doi.org/10.1007/s12079-021-00610-w.

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AbstractMuscular dystrophies (MDs) are a diverse group of severe disorders characterized by increased skeletal muscle feebleness. In many cases, respiratory and cardiac muscles are also compromised. Skeletal muscle inflammation and fibrosis are hallmarks of several skeletal muscle diseases, including MDs. Until now, several keys signaling pathways and factors that regulate inflammation and fibrosis have been identified. However, no curative treatments are available. Therefore, it is necessary to find new therapeutic targets to fight these diseases and improve muscle performance. Lysophosphatidic acid (LPA) is an active glycerophospholipid mainly synthesized by the secreted enzyme autotaxin (ATX), which activates six different G protein-coupled receptors named LPA1 to LPA6 (LPARs). In conjunction, they are part of the ATX/LPA/LPARs axis, involved in the inflammatory and fibrotic response in several organs-tissues. This review recapitulates the most relevant aspects of inflammation and fibrosis in MDs. It analyzes experimental evidence of the effects of the ATX/LPA/LPARs axis on inflammatory and fibrotic responses. Finally, we speculate about its potential role as a new therapeutic pharmacological target to treat these diseases.

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Choi, Alee, Sang Eon Park, Jang Bin Jeong, Suk-joo Choi, Soo-young Oh, Gyu Ha Ryu, Jeehun Lee, Hong Bae Jeon, and Jong Wook Chang. "Anti-Fibrotic Effect of Human Wharton’s Jelly-Derived Mesenchymal Stem Cells on Skeletal Muscle Cells, Mediated by Secretion of MMP-1." International Journal of Molecular Sciences 21, no. 17 (August 29, 2020): 6269. http://dx.doi.org/10.3390/ijms21176269.

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Extracellular matrix (ECM) components play an important role in maintaining skeletal muscle function, but excessive accumulation of ECM components interferes with skeletal muscle regeneration after injury, eventually inducing fibrosis. Increased oxidative stress level caused by dystrophin deficiency is a key factor in fibrosis in Duchenne muscular dystrophy (DMD) patients. Mesenchymal stem cells (MSCs) are considered a promising therapeutic agent for various diseases involving fibrosis. In particular, the paracrine factors secreted by MSCs play an important role in the therapeutic effects of MSCs. In this study, we investigated the effects of MSCs on skeletal muscle fibrosis. In 2–5-month-old mdx mice intravenously injected with 1 × 105 Wharton’s jelly (WJ)-derived MSCs (WJ-MSCs), fibrosis intensity and accumulation of calcium/necrotic fibers were significantly decreased. To elucidate the mechanism of this effect, we verified the effect of WJ-MSCs in a hydrogen peroxide-induced fibrosis myotubes model. In addition, we demonstrated that matrix metalloproteinase-1 (MMP-1), a paracrine factor, is critical for this anti-fibrotic effect of WJ-MSCs. These findings demonstrate that WJ-MSCs exert anti-fibrotic effects against skeletal muscle fibrosis, primarily via MMP-1, indicating a novel target for the treatment of muscle diseases, such as DMD.

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Yosef, Benyam, Yu Zhou, Kathryn Mouschouris, James Poteracki, Shay Soker, and Tracy Criswell. "N-Acetyl-L-Cysteine Reduces Fibrosis and Improves Muscle Function After Acute Compartment Syndrome Injury." Military Medicine 185, Supplement_1 (January 2020): 25–34. http://dx.doi.org/10.1093/milmed/usz232.

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ABSTRACT Introduction Upon injury, skeletal muscle undergoes a multiphase process beginning with degeneration of the damaged tissue, which is accompanied by inflammation and finally regeneration. One consequence of an injured microenvironment is excessive production of reactive oxygen species, which results in attenuated regeneration and recovery of function ultimately leading to fibrosis and disability. The objective of this research was to test the potential of the antioxidant, N-Acetyl-L-Cysteine (NAC), as a mediator of reactive oxygen species damage that results from traumatic muscle injury in order to support repair and regeneration of wounded muscle tissue and improve function recovery. Materials and Methods Adult female Lewis rats were subjected to compartment syndrome injury as previously published by our group. Rats received intramuscular injections of NAC or vehicle at 24, 48, and 72 hours postinjury. Muscle function, tissue fibrosis, and the expression of myogenic and angiogenic markers were measured. Results Muscle function was significantly improved, and tissue fibrosis was significantly decreased in NAC-treated muscles. Conclusions These results suggest that NAC treatment of skeletal muscle after injury may be a viable option for the prevention of long-term fibrosis and scar formation, facilitating recovery of muscle function.

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Rebolledo, Daniela L., María José Acuña, and Enrique Brandan. "Role of Matricellular CCN Proteins in Skeletal Muscle: Focus on CCN2/CTGF and Its Regulation by Vasoactive Peptides." International Journal of Molecular Sciences 22, no. 10 (May 15, 2021): 5234. http://dx.doi.org/10.3390/ijms22105234.

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The Cellular Communication Network (CCN) family of matricellular proteins comprises six proteins that share conserved structural features and play numerous biological roles. These proteins can interact with several receptors or soluble proteins, regulating cell signaling pathways in various tissues under physiological and pathological conditions. In the skeletal muscle of mammals, most of the six CCN family members are expressed during embryonic development or in adulthood. Their roles during the adult stage are related to the regulation of muscle mass and regeneration, maintaining vascularization, and the modulation of skeletal muscle fibrosis. This work reviews the CCNs proteins’ role in skeletal muscle physiology and disease, focusing on skeletal muscle fibrosis and its regulation by Connective Tissue Growth factor (CCN2/CTGF). Furthermore, we review evidence on the modulation of fibrosis and CCN2/CTGF by the renin-angiotensin system and the kallikrein-kinin system of vasoactive peptides.

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Trensz, Frédéric, Sonia Haroun, Alexandre Cloutier, Martin V. Richter, and Guillaume Grenier. "A muscle resident cell population promotes fibrosis in hindlimb skeletal muscles of mdx mice through the Wnt canonical pathway." American Journal of Physiology-Cell Physiology 299, no. 5 (November 2010): C939—C947. http://dx.doi.org/10.1152/ajpcell.00253.2010.

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Previous work has pointed to a role for the Wnt canonical pathway in fibrosis formation in aged skeletal muscles. In the present study, we studied the dystrophic mdx mouse, which displays skeletal muscle fibrosis. Our results indicated that the muscle resident stromal cell (mrSC) population in the muscles of dystrophic mice is higher than in the muscles of age-matched wild-type mice. Wnt3a promoted the proliferation of and collagen expression by cultured mrSCs but arrested the growth of and collagen expression by cultured myoblasts. Injections of Wnt3A in the tibialis anterior muscles of adult wild-type mice significantly enhanced the mrSC population and collagen deposition compared with the contralateral muscles. Conversely, an injection of the Wnt antagonist Dickkof protein (DKK1) into the skeletal muscles of mdx mice significantly reduced collagen deposition. These results suggested that the Wnt canonical pathway expands the population of mrSCs and stimulates their production of collagen as observed during aging and in various myopathies.

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Swaggart, Kayleigh A., Ahlke Heydemann, Abraham A. Palmer, and Elizabeth M. McNally. "Distinct genetic regions modify specific muscle groups in muscular dystrophy." Physiological Genomics 43, no. 1 (January 2011): 24–31. http://dx.doi.org/10.1152/physiolgenomics.00172.2010.

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Phenotypic expression in the muscular dystrophies is variable, even with the identical mutation, providing strong evidence that genetic modifiers influence outcome. To identify genetic modifier loci, we used quantitative trait locus mapping in two differentially affected mouse strains with muscular dystrophy. Using the Sgcg model of limb girdle muscular dystrophy that lacks the dystrophin-associated protein γ-sarcoglycan, we evaluated chromosomal regions that segregated with two distinct quantifiable characteristics of muscular dystrophy, membrane permeability and fibrosis. We previously identified a single major locus on murine chromosome 7 that influences both traits of membrane permeability and fibrosis in the quadriceps muscle. Using a larger cohort, we now found that this same interval strongly associated with both traits in all limb skeletal muscle groups studied, including the gastrocnemius/soleus, gluteus/hamstring, and triceps muscles. In contrast, the muscles of the trunk were modified by distinct genetic loci, possibly reflecting the embryological origins and physiological stressors unique to these muscle groups. A locus on chromosome 18 was identified that modified membrane permeability of the abdominal muscles, and a locus on chromosome 3 was found that regulated diaphragm and abdominal muscle fibrosis. Fibrosis in the heart associated with a region on chromosome 9 and likely reflects differential function between cardiac and skeletal muscle. These data underscore the complexity of inheritance and penetrance of single-gene disorders.

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Smith, Lucas R., and Elisabeth R. Barton. "Collagen content does not alter the passive mechanical properties of fibrotic skeletal muscle inmdxmice." American Journal of Physiology-Cell Physiology 306, no. 10 (May 15, 2014): C889—C898. http://dx.doi.org/10.1152/ajpcell.00383.2013.

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Many skeletal muscle diseases are associated with progressive fibrosis leading to impaired muscle function. Collagen within the extracellular matrix is the primary structural protein providing a mechanical scaffold for cells within tissues. During fibrosis collagen not only increases in amount but also undergoes posttranslational changes that alter its organization that is thought to contribute to tissue stiffness. Little, however, is known about collagen organization in fibrotic muscle and its consequences for function. To investigate the relationship between collagen content and organization with muscle mechanical properties, we studied mdx mice, a model for Duchenne muscular dystrophy (DMD) that undergoes skeletal muscle fibrosis, and age-matched control mice. We determined collagen content both histologically, with picosirius red staining, and biochemically, with hydroxyproline quantification. Collagen content increased in the mdx soleus and diaphragm muscles, which was exacerbated by age in the diaphragm. Collagen packing density, a parameter of collagen organization, was determined using circularly polarized light microscopy of picosirius red-stained sections. Extensor digitorum longus (EDL) and soleus muscle had proportionally less dense collagen in mdx muscle, while the diaphragm did not change packing density. The mdx muscles had compromised strength as expected, yet only the EDL had a significantly increased elastic stiffness. The EDL and diaphragm had increased dynamic stiffness and a change in relative viscosity. Unexpectedly, passive stiffness did not correlate with collagen content and only weakly correlated with collagen organization. We conclude that muscle fibrosis does not lead to increased passive stiffness and that collagen content is not predictive of muscle stiffness.

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Chan, Yi-Sheng, Yong Li, William Foster, Takashi Horaguchi, George Somogyi, Freddie H. Fu, and Johnny Huard. "Antifibrotic effects of suramin in injured skeletal muscle after laceration." Journal of Applied Physiology 95, no. 2 (August 2003): 771–80. http://dx.doi.org/10.1152/japplphysiol.00915.2002.

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Muscle injuries are very common in traumatology and sports medicine. Although muscle tissue can regenerate postinjury, the healing process is slow and often incomplete; complete recovery after skeletal muscle injury is hindered by fibrosis. Our studies have shown that decreased fibrosis could improve muscle healing. Suramin has been found to inhibit transforming growth factor (TGF)-β1 expression by competitively binding to the growth factor receptor. We conducted a series of tests to determine the antifibrotic effects of suramin on muscle laceration injuries. Our results demonstrate that suramin (50 μg/ml) can effectively decrease fibroblast proliferation and fibrotic-protein expression (α-smooth muscle actin) in vitro. In vivo, direct injection of suramin (2.5 mg) into injured murine muscle resulted in effective inhibition of muscle fibrosis and enhanced muscle regeneration, which led to efficient functional muscle recovery. These results support our hypothesis that prevention of fibrosis could enhance muscle regeneration, thereby facilitating more efficient muscle healing. This study could significantly contribute to the development of strategies to promote efficient muscle healing and functional recovery.

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Kharraz, Yacine, Joana Guerra, Patrizia Pessina, Antonio L. Serrano, and Pura Muñoz-Cánoves. "Understanding the Process of Fibrosis in Duchenne Muscular Dystrophy." BioMed Research International 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/965631.

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Fibrosis is the aberrant deposition of extracellular matrix (ECM) components during tissue healing leading to loss of its architecture and function. Fibrotic diseases are often associated with chronic pathologies and occur in a large variety of vital organs and tissues, including skeletal muscle. In human muscle, fibrosis is most readily associated with the severe muscle wasting disorder Duchenne muscular dystrophy (DMD), caused by loss of dystrophin gene function. In DMD, skeletal muscle degenerates and is infiltrated by inflammatory cells and the functions of the muscle stem cells (satellite cells) become impeded and fibrogenic cells hyperproliferate and are overactivated, leading to the substitution of skeletal muscle with nonfunctional fibrotic tissue. Here, we review new developments in our understanding of the mechanisms leading to fibrosis in DMD and several recent advances towards reverting it, as potential treatments to attenuate disease progression.

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Grabowska, Iwona, Malgorzata Zimowska, Karolina Maciejewska, Zuzanna Jablonska, Anna Bazga, Michal Ozieblo, Wladyslawa Streminska, Joanna Bem, Edyta Brzoska, and Maria Ciemerych. "Adipose Tissue-Derived Stromal Cells in Matrigel Impact the Regeneration of Severely Damaged Skeletal Muscles." International Journal of Molecular Sciences 20, no. 13 (July 5, 2019): 3313. http://dx.doi.org/10.3390/ijms20133313.

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In case of large injuries of skeletal muscles the pool of endogenous stem cells, i.e., satellite cells, might be not sufficient to secure proper regeneration. Such failure in reconstruction is often associated with loss of muscle mass and excessive formation of connective tissue. Therapies aiming to improve skeletal muscle regeneration and prevent fibrosis may rely on the transplantation of different types of stem cell. Among such cells are adipose tissue-derived stromal cells (ADSCs) which are relatively easy to isolate, culture, and manipulate. Our study aimed to verify applicability of ADSCs in the therapies of severely injured skeletal muscles. We tested whether 3D structures obtained from Matrigel populated with ADSCs and transplanted to regenerating mouse gastrocnemius muscles could improve the regeneration. In addition, ADSCs used in this study were pretreated with myoblasts-conditioned medium or anti-TGFβ antibody, i.e., the factors modifying their ability to proliferate, migrate, or differentiate. Analyses performed one week after injury allowed us to show the impact of 3D cultured control and pretreated ADSCs at muscle mass and structure, as well as fibrosis development immune response of the injured muscle.

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Birbrair, Alexander, Tan Zhang, Zhong-Min Wang, Maria Laura Messi, Akiva Mintz, and Osvaldo Delbono. "Type-1 pericytes participate in fibrous tissue deposition in aged skeletal muscle." American Journal of Physiology-Cell Physiology 305, no. 11 (December 1, 2013): C1098—C1113. http://dx.doi.org/10.1152/ajpcell.00171.2013.

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In older adults, changes in skeletal muscle composition are associated with increased fibrosis, loss of mass, and decreased force, which can lead to dependency, morbidity, and mortality. Understanding the biological mechanisms responsible is essential to sustaining and improving their quality of life. Compared with young mice, aged mice take longer to recover from muscle injury; their tissue fibrosis is more extensive, and regenerated myofibers are smaller. Strong evidence indicates that cells called pericytes, embedded in the basement membrane of capillaries, contribute to the satellite-cell pool and muscle growth. In addition to their role in skeletal muscle repair, after tissue damage, they detach from capillaries and migrate to the interstitial space to participate in fibrosis formation. Here we distinguish two bona fide pericyte subtypes in the skeletal muscle interstitium, type-1 (Nestin-GFP−/NG2-DsRed+) and type-2 (Nestin-GFP+/NG2-DsRed+), and characterize their heretofore unknown specific roles in the aging environment. Our in vitro results show that type-1 and type-2 pericytes are either fibrogenic or myogenic, respectively. Transplantation studies in young animals indicate that type-2 pericytes are myogenic, while type-1 pericytes remain in the interstitial space. In older mice, however, the muscular regenerative capacity of type-2 pericytes is limited, and type-1 pericytes produce collagen, contributing to fibrous tissue deposition. We conclude that in injured muscles from aging mice, the pericytes involved in skeletal muscle repair differ from those associated with scar formation.

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Ismaeel, Ahmed, Jeong-Su Kim, Jeffrey S. Kirk, Robert S. Smith, William T. Bohannon, and Panagiotis Koutakis. "Role of Transforming Growth Factor-β in Skeletal Muscle Fibrosis: A Review." International Journal of Molecular Sciences 20, no. 10 (May 17, 2019): 2446. http://dx.doi.org/10.3390/ijms20102446.

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Transforming growth factor-beta (TGF-β) isoforms are cytokines involved in a variety of cellular processes, including myofiber repair and regulation of connective tissue formation. Activation of the TGF-β pathway contributes to pathologic fibrosis in most organs. Here, we have focused on examining the evidence demonstrating the involvement of TGF-β in the fibrosis of skeletal muscle particularly. The TGF-β pathway plays a role in different skeletal muscle myopathies, and TGF-β signaling is highly induced in these diseases. In this review, we discuss different molecular mechanisms of TGF-β-mediated skeletal muscle fibrosis and highlight different TGF-β-targeted treatments that target these relevant pathways.

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Yan, Mingyang, Rongguo Wang, Shouyao Liu, Ying Chen, Peng Lin, Tengqi Li, and Yunting Wang. "The Mechanism of Electroacupuncture at Zusanli Promotes Macrophage Polarization during the Fibrotic Process in Contused Skeletal Muscle." European Surgical Research 60, no. 5-6 (2019): 196–207. http://dx.doi.org/10.1159/000503130.

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Introduction: Currently, many clinical experiments are being conducted to study the effect of acupuncture on skeletal muscle contusions, and its therapeutic effect has been confirmed to some extent. However, the mechanism of recovery by electroacupuncture (EA) in skeletal muscles after blunt trauma remains unknown. Objective: To determine whether EA at Zusanli can contribute to the regeneration of contused skeletal muscle and the molecular mechanism involved. Methods: Masson’s trichrome staining and hematoxylin and eosin staining were used to measure the area of fibrotic tissue and determine the number of centrally nucleated muscle fibers respectively. The different immune phenotypes of macrophages were determined by flow cytometry. Then, ELISA was used to analyze the levels of interleukin-4 (IL-4), IL-6, interferon-α (IFN-α) and interferon-γ (IFN-γ) in the injured tissue. Finally, the expression of MyoD in the tissue was detected by quantitative real-time polymerase chain reaction. Results: EA at Zusanli helped regenerate contused skeletal muscle by alleviating fibrosis and increasing the size of the regenerating myofibres in the injured skeletal muscle. EA at Zusanli increased the number of M2 macrophages and decreased the number of M1 macrophages in contused skeletal muscle. EA at Zusanli decreased the level of cytokine IFN-γ and increased the levels of IL-4, interleukin-13 (IL-13), and IFN-α, which promoted macrophage polarization during the fibrosis recovery process in the contused skeletal muscle. EA at Zusanli could increase the expression of MyoD in tissues. Conclusions: EA at Zusanli promoted macrophage polarization during the fibrotic process in contused skeletal muscle by decreasing cytokine IFN-γ and increasing IL-4, IL-13, and IFN-α, which contributed to the regeneration of the contused skeletal muscle.

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Negishi, Shinichi, Yong Li, Arvydas Usas, Freddie H. Fu, and Johnny Huard. "The Effect of Relaxin Treatment on Skeletal Muscle Injuries." American Journal of Sports Medicine 33, no. 12 (December 2005): 1816–24. http://dx.doi.org/10.1177/0363546505278701.

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Background Injured skeletal muscle can repair itself via spontaneous regeneration; however, the overproduction of extracellular matrix and excessive collagen deposition lead to fibrosis. Neutralization of the effect of transforming growth factor-β1, a key fibrotic cytokine, on myogenic cell differentiation after muscle injury can prevent fibrosis, enhance muscle regeneration, and thereby improve the functional recovery of injured muscle. Hypothesis The hormone relaxin, a member of the family of insulin-like growth factors, can act as an antifibrosis agent and improve the healing of injured muscle. Study Design Controlled laboratory study. Methods In vitro: Myoblasts (C2C12 cells) and myofibroblasts (transforming growth factor-β1-transfected myoblasts) were incubated with relaxin, and cell growth and differentiation were examined. Myogenic and fibrotic protein expression was determined by Western blot analysis. In vivo: Relaxin was injected intramuscularly at different time points after laceration injury. Skeletal muscle healing was evaluated via histologic, immunohistochemical, and physiologic tests. Results Relaxin treatment resulted in a dose-dependent decrease in myofibroblast proliferation, down-regulated expression of the fibrotic protein α-smooth muscle actin, and promoted the proliferation and differentiation of myoblasts in vitro. Relaxin therapy enhanced muscle regeneration, reduced fibrosis, and improved injured muscle strength in vivo. Conclusion Administration of relaxin can significantly improve skeletal muscle healing. Clinical Relevance These findings may facilitate the development of techniques to eliminate fibrosis, enhance muscle regeneration, and improve functional recovery after muscle injuries.

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Iqbal, Aqsa, Ulrike May, Stuart N. Prince, Tero A. H. Järvinen, and Ahlke Heydemann. "Systemically Administered Homing Peptide Targets Dystrophic Lesions and Delivers Transforming Growth Factor-β (TGFβ) Inhibitor to Attenuate Murine Muscular Dystrophy Pathology." Pharmaceutics 13, no. 9 (September 18, 2021): 1506. http://dx.doi.org/10.3390/pharmaceutics13091506.

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Muscular dystrophy is a progressively worsening and lethal disease, where accumulation of functionality-impairing fibrosis plays a key pathogenic role. Transforming growth factor-β1 (TGFβ1) is a central signaling molecule in the development of fibrosis in muscular dystrophic humans and mice. Inhibition of TGFβ1 has proven beneficial in mouse models of muscular dystrophy, but the global strategies of TGFβ1 inhibition produce significant detrimental side effects. Here, we investigated whether murine muscular dystrophy lesion-specific inhibition of TGFβ1 signaling by the targeted delivery of therapeutic decorin (a natural TGFβ inhibitor) by a vascular homing peptide CAR (CARSKNKDC) would reduce skeletal muscle fibrosis and pathology and increase functional characteristics of skeletal muscle. We demonstrate that CAR peptide homes to dystrophic lesions with specificity in two muscular dystrophy models. Recombinant fusion protein consisting of CAR peptide and decorin homes selectively to sites of skeletal muscle damage in mdxDBA2/J and gamma-sarcoglycan deficient DBA2/J mice. This targeted delivery reduced TGFβ1 signaling as demonstrated by reduced nuclear pSMAD staining. Three weeks of targeted decorin treatment decreased both membrane permeability and fibrosis and improved skeletal muscle function in comparison to control treatments in the mdxD2 mice. These results show that selective delivery of decorin to the sites of skeletal muscle damage attenuates the progression of murine muscular dystrophy.

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Huebner, Kyla D., Davinder S. Jassal, Orna Halevy, Mark Pines, and Judy E. Anderson. "Functional resolution of fibrosis in mdx mouse dystrophic heart and skeletal muscle by halofuginone." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 4 (April 2008): H1550—H1561. http://dx.doi.org/10.1152/ajpheart.01253.2007.

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The effect of halofuginone (Halo) on established fibrosis in older mdx dystrophic muscle was investigated. Mice (8 to 9 mo) treated with Halo (or saline in controls) for 5, 10, or 12 wk were assessed weekly for grip strength and voluntary running. Echocardiography was performed at 0, 5, and 10 wk. Respiratory function and exercise-induced muscle damage were tested. Heart, quadriceps, diaphragm, and tibialis anterior muscles were collected to study fibrosis, collagen I and III expression, collagen content using a novel collagenase-digestion method, and cell proliferation. Hepatocyte growth factor and α-smooth muscle actin proteins were assayed in quadriceps. Halo decreased fibrosis (diaphragm and quadriceps), collagen I and III expression, collagen protein, and smooth muscle actin content after 10 wk treatment. Muscle-cell proliferation increased at 5 wk, and hepatocyte growth factor increased by 10 wk treatment. Halo markedly improved both cardiac and respiratory function and reduced damage and improved recovery from exercise. The overall impact of established dystrophy and dysfunction in cardiac and skeletal muscles was reduced by Halo treatment. Marked improvements in vital-organ functions implicate Halo as a strong candidate drug to reduce morbidity and mortality in Duchenne muscular dystrophy.

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Barry, Sinead C., and Charles G. Gallagher. "Corticosteroids and skeletal muscle function in cystic fibrosis." Journal of Applied Physiology 95, no. 4 (October 2003): 1379–84. http://dx.doi.org/10.1152/japplphysiol.00506.2002.

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Patients with cystic fibrosis (CF) have reduced peripheral muscle strength. We tested the hypothesis that steroid treatment contributes to muscle weakness in adults with CF. Twenty-three stable CF patients were studied. Measurements included knee extensor (KE), knee flexor (KF), elbow flexor (EF), handgrip (HG), expiratory (Pemax), and inspiratory (Pimax) muscle strengths. Spirometry, body mass index (BMI), and days spent in hospital over the preceding 12 mo (DH) were also measured. Average daily dose of prednisolone over the preceding 12 mo (ADD) was 5.1 mg/day. Pearson's correlation analysis revealed that ADD correlated significantly with skeletal muscle strengths (KF%, r = -0.63, P < 0.01) with the exception of HG%. These findings are independent of age, BMI, pulmonary function, and DH. Multiple-regression analysis revealed that ADD was the most significant predictor of all measures of skeletal muscle function except HG%. It was independently responsible for 54% of the variance in Pimax%, for 46% of the variance in Pemax%, for 45% of the variance in KE%, for 39% of the variance in KF%, and for 41% of the variance in EF%. Concomitant medications (e.g., theophylline) were shown to have no causative effect. Corticosteroids contribute to the skeletal muscle weakness seen in CF patients. The correlation of proximal muscle strength, but not HG strength, with steroid dosage further supports a cause-effect relationship.

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Akpulat, Uğur, İlyas Onbaşılar, and Y. Çetin Kocaefe. "Tenotomy immobilization as a model to investigate skeletal muscle fibrosis (with emphasis on Secreted frizzled-related protein 2)." Physiological Genomics 48, no. 6 (June 2016): 397–408. http://dx.doi.org/10.1152/physiolgenomics.00010.2016.

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The pathological endpoint of congenital and senile myopathies is chronic muscle degeneration characterized by the atrophy of contractile elements, accompanied by fibrosis and fatty infiltration of the interstitium. Tenotomy is the release of preload that causes abrupt shortening of the muscle and models atrophy and fibrosis without prominent inflammatory response. Fibrosis in the skeletal muscle is known to be triggered by transforming growth factor (TGF)-β, which is activated by inflammatory events. As these were lacking, tenotomy provided an opportunity to investigate transcriptional events on a background without inflammation. An unbiased look at the transcriptome of tenotomy-immobilized soleus muscle revealed that the majority of the transcriptional changes took place in the first 4 wk. Regarding atrophy, proteasomal and lysosomal pathways were actively involved in accompanying cathepsins and calpains in the breakdown of the macromolecular contractile machinery. The transcriptome provided clear-cut evidence for the upregulation of collagens and several extracellular matrix components that define fibrotic remodeling of the skeletal muscle architecture as well as activation of the fibro-adipogenic precursors. Concomitantly, Sfrp2, a Wnt antagonist as well as a procollagen processor, accompanied fibrosis in skeletal muscle with an expression that was stringently confined to the slow-twitch fibers. An interpreted mechanistic scenario construed the kinetic events initiated through the abnormal shortening of the muscle fibers as enough to trigger the resident latent TGF-β in the extracellular matrix, leading to the activation of fibroadipogenic precursors. As in the heart, Sfrp2 shows itself to be a therapeutic target for the prevention of irreversible fibrosis in degenerative skeletal muscle conditions.

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Morris, C. A., J. T. Selsby, L. D. Morris, K. Pendrak, and H. L. Sweeney. "Bowman-Birk inhibitor attenuates dystrophic pathology in mdx mice." Journal of Applied Physiology 109, no. 5 (November 2010): 1492–99. http://dx.doi.org/10.1152/japplphysiol.01283.2009.

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Bowman-Birk inhibitor concentrate (BBIC), a serine protease inhibitor, has been shown to diminish disuse atrophy of skeletal muscle. Duchenne muscular dystrophy (DMD) results from a loss of dystrophin protein and involves an ongoing inflammatory response, with matrix remodeling and activation of transforming growth factor (TGF)-β1 leading to tissue fibrosis. Inflammatory-mediated increases in extracellular protease activity may drive much of this pathological tissue remodeling. Hence, we evaluated the ability of BBIC, an extracellular serine protease inhibitor, to impact pathology in the mouse model of DMD (mdx mouse). Mdx mice fed 1% BBIC in their diet had increased skeletal muscle mass and tetanic force and improved muscle integrity (less Evans blue dye uptake). Importantly, mdx mice treated with BBIC were less susceptible to contraction-induced injury. Changes consistent with decreased degeneration/regeneration, as well as reduced TGF-β1 and fibrosis, were observed in the BBIC-treated mdx mice. While Akt signaling was unchanged, myostatin activitation and Smad signaling were reduced. Given that BBIC treatment increases mass and strength, while decreasing fibrosis in skeletal muscles of the mdx mouse, it should be evaluated as a possible therapeutic to slow the progression of disease in human DMD patients.

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Whitehead, Nicholas P., Min Jeong Kim, Kenneth L. Bible, Marvin E. Adams, and Stanley C. Froehner. "A new therapeutic effect of simvastatin revealed by functional improvement in muscular dystrophy." Proceedings of the National Academy of Sciences 112, no. 41 (September 28, 2015): 12864–69. http://dx.doi.org/10.1073/pnas.1509536112.

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Duchenne muscular dystrophy (DMD) is a lethal, degenerative muscle disease with no effective treatment. DMD muscle pathogenesis is characterized by chronic inflammation, oxidative stress, and fibrosis. Statins, cholesterol-lowering drugs, inhibit these deleterious processes in ischemic diseases affecting skeletal muscle, and therefore have potential to improve DMD. However, statins have not been considered for DMD, or other muscular dystrophies, principally because skeletal-muscle-related symptoms are rare, but widely publicized, side effects of these drugs. Here we show positive effects of statins in dystrophic skeletal muscle. Simvastatin dramatically reduced damage and enhanced muscle function in dystrophic (mdx) mice. Long-term simvastatin treatment vastly improved overall muscle health inmdxmice, reducing plasma creatine kinase activity, an established measure of muscle damage, to near-normal levels. This reduction was accompanied by reduced inflammation, more oxidative muscle fibers, and improved strength of the weak diaphragm muscle. Shorter-term treatment protected against muscle fatigue and increasedmdxhindlimb muscle force by 40%, a value comparable to current dystrophin gene-based therapies. Increased force correlated with reduced NADPH Oxidase 2 protein expression, the major source of oxidative stress in dystrophic muscle. Finally, in oldmdxmice with severe muscle degeneration, simvastatin enhanced diaphragm force and halved fibrosis, a major cause of functional decline in DMD. These improvements were accompanied by autophagy activation, a recent therapeutic target for DMD, and less oxidative stress. Together, our findings highlight that simvastatin substantially improves the overall health and function of dystrophic skeletal muscles and may provide an unexpected, novel therapy for DMD and related neuromuscular diseases.

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Gibson, Sarah E., Carol F. Farver, and Richard A. Prayson. "Multiorgan Involvement in Nephrogenic Fibrosing Dermopathy: An Autopsy Case and Review of the Literature." Archives of Pathology & Laboratory Medicine 130, no. 2 (February 1, 2006): 209–12. http://dx.doi.org/10.5858/2006-130-209-miinfd.

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Abstract Nephrogenic fibrosing dermopathy is a recently recognized, scleromyxedema-like fibrosing skin condition that occurs in individuals with acute or chronic renal failure. Although the early descriptions of this disorder describe a purely cutaneous disease process, 2 recent autopsy reports have identified apparent multiorgan fibrosis with involvement of skeletal muscle, myocardium, lungs, kidneys, and testes. We describe a 23-year-old man with nephrogenic fibrosing dermopathy and significant fibrosis of the atrial myocardium and dura mater, which was identified at autopsy. Dural fibrosis is a previously undescribed systemic manifestation of nephrogenic fibrosing dermopathy. The literature is reviewed.

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Rosero Salazar, D. H., P. L. Carvajal Monroy, F. A. D. T. G. Wagener, and J. W. Von den Hoff. "Orofacial Muscles: Embryonic Development and Regeneration after Injury." Journal of Dental Research 99, no. 2 (November 1, 2019): 125–32. http://dx.doi.org/10.1177/0022034519883673.

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Orofacial congenital defects such as cleft lip and/or palate are associated with impaired muscle regeneration and fibrosis after surgery. Also, other orofacial reconstructions or trauma may end up in defective muscle regeneration and fibrosis. The aim of this review is to discuss current knowledge on the development and regeneration of orofacial muscles in comparison to trunk and limb muscles. The orofacial muscles include the tongue muscles and the branchiomeric muscles in the lower face. Their main functions are chewing, swallowing, and speech. All orofacial muscles originate from the mesoderm of the pharyngeal arches under the control of cranial neural crest cells. Research in vertebrate models indicates that the molecular regulation of orofacial muscle development is different from that of trunk and limb muscles. In addition, the regenerative ability of orofacial muscles is lower, and they develop more fibrosis than other skeletal muscles. Therefore, specific approaches need to be developed to stimulate orofacial muscle regeneration. Regeneration may be stimulated by growth factors such fibroblast growth factors and hepatocyte growth factor, while fibrosis may be reduced by targeting the transforming growth factor β1 (TGFβ1)/myofibroblast axis. New approaches that combine these 2 aspects will improve the surgical treatment of orofacial muscle defects.

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Stepien, David M., Charles Hwang, Simone Marini, Chase A. Pagani, Michael Sorkin, Noelle D. Visser, Amanda K. Huber, et al. "Tuning Macrophage Phenotype to Mitigate Skeletal Muscle Fibrosis." Journal of Immunology 204, no. 8 (March 11, 2020): 2203–15. http://dx.doi.org/10.4049/jimmunol.1900814.

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Barry, S. C., and C. G. Gallagher. "Corticosteroids and Skeletal Muscle Function in Cystic Fibrosis." Cardiopulmonary Physical Therapy Journal 15, no. 1 (March 2004): 30. http://dx.doi.org/10.1097/01823246-200415010-00014.

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Jong, Wietze de, Wim M. C. van Aalderen, Jan Kraan, Gerard H. Koëter, and Cees P. van der Schans. "Skeletal muscle strength in patients with cystic fibrosis." Physiotherapy Theory and Practice 17, no. 1 (January 2001): 23–28. http://dx.doi.org/10.1080/09593980151143237.

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Zanotti, S., S. Gibertini, F. Blasevich, S. Saredi, C. Bragato, A. Ruggieri, R. Mantegazza, L. Maggi, and M. Mora. "Potential role of exosomes in skeletal muscle fibrosis." Neuromuscular Disorders 27 (October 2017): S169. http://dx.doi.org/10.1016/j.nmd.2017.06.275.

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Serrano, Antonio L., and Pura Muñoz-Cánoves. "Regulation and dysregulation of fibrosis in skeletal muscle." Experimental Cell Research 316, no. 18 (November 2010): 3050–58. http://dx.doi.org/10.1016/j.yexcr.2010.05.035.

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Mann, Christopher J., Eusebio Perdiguero, Yacine Kharraz, Susana Aguilar, Patrizia Pessina, Antonio L. Serrano, and Pura Muñoz-Cánoves. "Aberrant repair and fibrosis development in skeletal muscle." Skeletal Muscle 1, no. 1 (2011): 21. http://dx.doi.org/10.1186/2044-5040-1-21.

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Matsumoto, Yoshinari, Hideki Fujii, Mika Harima, Haruna Okamura, Yoshimi Yukawa-Muto, Naoshi Odagiri, Hiroyuki Motoyama, et al. "Severity of Liver Fibrosis Is Associated with the Japanese Diet Pattern and Skeletal Muscle Mass in Patients with Nonalcoholic Fatty Liver Disease." Nutrients 15, no. 5 (February 26, 2023): 1175. http://dx.doi.org/10.3390/nu15051175.

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It is not fully clear as to which dietary patterns are associated with the pathogenesis of nonalcoholic fatty liver disease (NAFLD) in Asia. We conducted a cross-sectional study of 136 consecutively recruited patients with NAFLD (49% female, median age 60 years). Severity of liver fibrosis was assessed using the Agile 3+ score, a recently proposed system based on vibration-controlled transient elastography. Dietary status was assessed using the 12-component modified Japanese diet pattern index (mJDI12). Skeletal muscle mass was assessed by bioelectrical impedance. Factors associated with intermediate–high-risk Agile 3+ scores and skeletal muscle mass (75th percentile or higher) were analyzed by multivariable logistic regression. After adjustment for confounders, such as age and sex, the mJDI12 (OR: 0.77; 95% CI: 0.61, 0.99) and skeletal muscle mass (75th percentile or higher) (OR: 0.23; 95% CI: 0.07, 0.77) were significantly associated with intermediate–high-risk Agile 3+ scores. Soybeans and soybean foods were significantly associated with skeletal muscle mass (75th percentile or higher) (OR: 1.02; 95% CI: 1.00, 1.04). In conclusion, the Japanese diet pattern was associated with the severity of liver fibrosis in Japanese patients with NAFLD. Skeletal muscle mass was also associated with the severity of liver fibrosis, and intake of soybeans and soybean foods.

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Cheng, Naixuan, Chang Liu, Yulin Li, Shijuan Gao, Ying-Chun Han, Xiaonan Wang, Jie Du, and Congcong Zhang. "MicroRNA-223-3p promotes skeletal muscle regeneration by regulating inflammation in mice." Journal of Biological Chemistry 295, no. 30 (June 3, 2020): 10212–23. http://dx.doi.org/10.1074/jbc.ra119.012263.

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After injury, the coordinated balance of pro- and anti-inflammatory factors in the microenvironment contribute to skeletal muscle regeneration. However, the underlying molecular mechanisms regulating this balance remain incompletely understood. In this study, we examined the roles of microRNAs (miRNAs) in inflammation and muscle regeneration. miRNA-Seq transcriptome analysis of mouse skeletal muscle revealed that miR-223-3p is upregulated in the early stage of muscle regeneration after injury. miR-223-3p knockout resulted in increased inflammation, impaired muscle regeneration, and increased interstitial fibrosis. Mechanistically, we found that myeloid-derived miR-223-3p suppresses the target gene interleukin-6 (Il6), associated with the maintenance of the proinflammatory macrophage phenotype during injury. Administration of IL-6-neutralizing antibody in miR-223-3p-knockout muscle could rescue the impaired regeneration ability and reduce the fibrosis. Together, our results reveal that miR-223-3p improves muscle regeneration by regulating inflammation, indicating that miRNAs can participate in skeletal muscle regeneration by controlling the balance of pro- and anti-inflammatory factors in the skeletal muscle microenvironment.

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Howard, Zachary M., Neha Rastogi, Jeovanna Lowe, J. Spencer Hauck, Pratham Ingale, Chetan Gomatam, Celso E. Gomez-Sanchez, Elise P. Gomez-Sanchez, Shyam S. Bansal, and Jill A. Rafael-Fortney. "Myeloid mineralocorticoid receptors contribute to skeletal muscle repair in muscular dystrophy and acute muscle injury." American Journal of Physiology-Cell Physiology 322, no. 3 (March 1, 2022): C354—C369. http://dx.doi.org/10.1152/ajpcell.00411.2021.

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Suppressing mineralocorticoid receptor (MR) activity with MR antagonists is therapeutic for chronic skeletal muscle pathology in Duchenne muscular dystrophy (DMD) mouse models. Although mechanisms underlying clinical MR antagonist efficacy for DMD cardiomyopathy and other cardiac diseases are defined, mechanisms in skeletal muscles are not fully elucidated. Myofiber MR knockout improves skeletal muscle force and a subset of dystrophic pathology. However, MR signaling in myeloid cells is known to be a major contributor to cardiac efficacy. To define contributions of myeloid MR in skeletal muscle function and disease, we performed parallel assessments of muscle pathology, cytokine levels, and myeloid cell populations resulting from myeloid MR genetic knockout in muscular dystrophy and acute muscle injury. Myeloid MR knockout led to lower levels of C-C motif chemokine receptor 2 (CCR2)-expressing macrophages, resulting in sustained myofiber damage after acute injury of normal muscle. In acute injury, myeloid MR knockout also led to increased local muscle levels of the enzyme that produces the endogenous MR agonist aldosterone, further supporting important contributions of MR signaling in normal muscle repair. In muscular dystrophy, myeloid MR knockout altered cytokine levels differentially between quadriceps and diaphragm muscles, which contain different myeloid populations. Myeloid MR knockout led to higher levels of fibrosis in dystrophic diaphragm. These results support important contributions of myeloid MR signaling to skeletal muscle repair in acute and chronic injuries and highlight the useful information gained from cell-specific genetic knockouts to delineate mechanisms of pharmacological efficacy.

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Baltzer, Wendy Irene, David V. Calise, Jonathan M. Levine, G. D. Shelton, John F. Edwards, and Joerg M. Steiner. "Dystrophin-Deficient Muscular Dystrophy in a Weimaraner." Journal of the American Animal Hospital Association 43, no. 4 (July 1, 2007): 227–32. http://dx.doi.org/10.5326/0430227.

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A 2-year-old, male Weimaraner with muscular dystrophy was presented with generalized muscle atrophy of the limbs; hypertrophy of the neck, infraspinatus, and lingual muscles; dysphagia; and regurgitation. Unilateral cryptorchidism, unilateral renal agenesis, and hiatal hernia were also detected. Spontaneous muscle activity was identified on myography. Serum creatine kinase was markedly elevated. Immunohistochemical staining for dystrophin was restricted to suspected revertant (characteristics of immaturity) fibers. Histologically, skeletal myofiber degeneration, endomysial fibrosis, and mineralization were present. Following euthanasia, necropsy revealed hypertrophy of the diaphragm and cardiac muscle fibrosis. This case of muscular dystrophy represents a slowly progressive form with organ agenesis.

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Ibrahim, Abdalla, Eoghan Meagher, Alexander Fraser, and Thomas J. Kiernan. "A Young Male with Severe Myocarditis and Skeletal Muscle Myositis." Case Reports in Cardiology 2018 (June 14, 2018): 1–4. http://dx.doi.org/10.1155/2018/5698739.

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A 34-year-old male presented with retrosternal chest pain, fatigue, shortness of breath, and a history of a previous episode of myocarditis four years prior. He had elevated troponin T, normal skeletal muscle enzymes, and negative inflammatory markers. Cardiac magnetic resonance imaging (MRI) confirmed active myocarditis with extensive myocardial fibrosis and normal left ventricular ejection fraction (LVEF). His myocarditis symptoms resolved with steroids and anti-inflammatory treatment, but on closer questioning, he reported a vague history of long-standing calf discomfort associated with episodes of stiffness, fatigue, and flu-like symptoms. MRI of the lower legs consequently demonstrated active myositis in the calf muscles. Immunomodulatory therapy was commenced with good effect. The patient is undergoing regular follow-up in both cardiology and rheumatology outpatient departments. Repeated MRI of the legs showed significant interval improvement in his skeletal muscle myositis, and repeat cardiac MRI demonstrated the resolution of myocarditis along with persistent stable extensive myocardial fibrosis and preserved LVEF. The patient has returned to full-time work.

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Wang, Yanjie, Jianqiang Lu, and Yujian Liu. "Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models." International Journal of Molecular Sciences 23, no. 21 (November 2, 2022): 13380. http://dx.doi.org/10.3390/ijms232113380.

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Skeletal muscle injuries occur frequently in daily life and exercise. Understanding the mechanisms of regeneration is critical for accelerating the repair and regeneration of muscle. Therefore, this article reviews knowledge on the mechanisms of skeletal muscle regeneration after cardiotoxin-induced injury. The process of regeneration is similar in different mouse strains and is inhibited by aging, obesity, and diabetes. Exercise, microcurrent electrical neuromuscular stimulation, and mechanical loading improve regeneration. The mechanisms of regeneration are complex and strain-dependent, and changes in functional proteins involved in the processes of necrotic fiber debris clearance, M1 to M2 macrophage conversion, SC activation, myoblast proliferation, differentiation and fusion, and fibrosis and calcification influence the final outcome of the regenerative activity.

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Laws, Nicola, Renée A. Cornford-Nairn, Nicole Irwin, Russell Johnsen, Susan Fletcher, Stephen D. Wilton, and Andrew J. Hoey. "Long-term administration of antisense oligonucleotides into the paraspinal muscles of mdx mice reduces kyphosis." Journal of Applied Physiology 105, no. 2 (August 2008): 662–68. http://dx.doi.org/10.1152/japplphysiol.00068.2008.

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The mdx mouse model of muscular dystrophy has a premature stop codon preventing production of dystrophin. This results in a progressive phenotype causing centronucleation of skeletal muscle fibers, muscle weakness, and fibrosis and kyphosis. Antisense oligonucleotides alter RNA splicing to exclude the nonsense mutation, while still maintaining the open reading frame to produce a shorter, but partially functional dystrophin protein that should ameliorate the extent of pathology. The present study investigated the benefits of chronic treatment of mdx mice by once-monthly deep intramuscular injections of antisense oligonucleotides into paraspinal muscles. After 8 mo of treatment, mdx mice had reduced development of kyphosis relative to untreated mdx mice, a benefit that was retained until completion of the study at 18 mo of age (16 mo of treatment). This was accompanied by reduced centronucleation in the latissimus dorsi and intercostals muscles and reduced fibrosis in the diaphragm and latissimus dorsi. These benefits were accompanied by a significant increase in dystrophin production. In conclusion, chronic antisense oligonucleotide treatment provides clear and ongoing benefits to paralumbar skeletal muscle, with associated marked reduction in kyphosis.

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Gardner, Tyler, Keith Kenter, and Yong Li. "Fibrosis following Acute Skeletal Muscle Injury: Mitigation and Reversal Potential in the Clinic." Journal of Sports Medicine 2020 (September 1, 2020): 1–7. http://dx.doi.org/10.1155/2020/7059057.

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Skeletal muscle injuries occur often in athletics and in daily life. In minor injuries, muscles are able to regenerate completely and recover their functional capabilities. However, in the case of severe injuries, the injured muscle cannot recover to a functional level because of the formation of fibrous scar tissue. The physical barrier of scars is significantly challenged in both research and clinical treatment. Fibrous scar tissue not only limits cells’ migration, but also contributes to normal tissue biomechanical properties. This scar formation creates an unsuitable environment for tissue structure resulting in frequent pain. Antifibrosis treatment is one of the major strategies used to augment muscle regeneration and accelerate its functional recovery. This review will discuss the currently available methods for improving muscle regeneration with a specific focus on antifibrosis applications. We also discussed several novel hypotheses and clinical applications in muscle fibrosis treatment currently in practice.

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Levine, Joshua M., Robert A. Taylor, Lauren B. Elman, Shawn J. Bird, Ehud Lavi, Ethan D. Stolzenberg, Michael L. McGarvey, Arthur K. Asbury, and Sergio A. Jimenez. "Involvement of skeletal muscle in dialysis-associated systemic fibrosis (nephrogenic fibrosing dermopathy)." Muscle & Nerve 30, no. 5 (October 19, 2004): 569–77. http://dx.doi.org/10.1002/mus.20153.

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Urso, Maria L. "Anti-inflammatory interventions and skeletal muscle injury: benefit or detriment?" Journal of Applied Physiology 115, no. 6 (September 15, 2013): 920–28. http://dx.doi.org/10.1152/japplphysiol.00036.2013.

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Exercise, eccentric contractions, acute trauma, and disease are all causal mechanisms of skeletal muscle injury. After skeletal muscle is injured, it undergoes sequential phases of degeneration, inflammation, regeneration, and fibrosis. Events that occur in response to inflammation trigger regenerative processes. However, since inflammation causes pain, decreases skeletal muscle function, has a negative effect on performance, and contributes to fibrosis, which is one of the leading causes of delayed regeneration, the general practice has been to reduce inflammation. The problem with this approach is that preventing inflammation may hinder recovery. Current treatment options for inflammation are not necessarily effective and, in some cases, they may be unsafe. This review focuses on the question of whether the most beneficial course of treatment should be to block inflammation or if it is sensible to allow inflammatory processes to progress naturally. If blocking inflammation is perceived as a beneficial approach, it is not yet known at what time point during the inflammatory response it is most sensible to interfere. To address these issues, this review evaluates the effects of various anti-inflammatory agents on recovery processes in response to exercise-induced, traumatic, and disease-associated models of skeletal muscle injury. A collective analysis such as this should lay the foundation for future work that systematically manipulates the inflammatory response to most effectively promote regeneration and functional recovery in injured skeletal muscle, while reducing the negative effects of inflammatory processes such as pain and fibrosis.

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Takahashi, Yuya, Tatsunori Shimizu, Shunsuke Kato, Mitsuhiko Nara, Yumi Suganuma, Takehiro Sato, Tsukasa Morii, Yuichiro Yamada, and Hiroki Fujita. "Reduction of Superoxide Dismutase 1 Delays Regeneration of Cardiotoxin-Injured Skeletal Muscle in KK/Ta-Ins2Akita Mice with Progressive Diabetic Nephropathy." International Journal of Molecular Sciences 22, no. 11 (May 23, 2021): 5491. http://dx.doi.org/10.3390/ijms22115491.

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Superoxide dismutase (SOD) is a major antioxidant enzyme for superoxide removal, and cytoplasmic SOD (SOD1) is expressed as a predominant isoform in all cells. We previously reported that renal SOD1 deficiency accelerates the progression of diabetic nephropathy (DN) via increasing renal oxidative stress. To evaluate whether the degree of SOD1 expression determines regeneration capacity and sarcopenic phenotypes of skeletal muscles under incipient and advanced DN conditions, we investigated the alterations of SOD1 expression, oxidative stress marker, inflammation, fibrosis, and regeneration capacity in cardiotoxin (CTX)-injured tibialis anterior (TA) muscles of two Akita diabetic mouse models with different susceptibility to DN, DN-resistant C57BL/6-Ins2Akita and DN-prone KK/Ta-Ins2Akita mice. Here, we report that KK/Ta-Ins2Akita mice, but not C57BL/6-Ins2Akita mice, exhibit delayed muscle regeneration after CTX injection, as demonstrated by the finding indicating significantly smaller average cross-sectional areas of regenerating TA muscle myofibers relative to KK/Ta-wild-type mice. Furthermore, we observed markedly reduced SOD1 expression in CTX-injected TA muscles of KK/Ta-Ins2Akita mice, but not C57BL/6-Ins2Akita mice, along with increased inflammatory cell infiltration, prominent fibrosis and superoxide overproduction. Our study provides the first evidence that SOD1 reduction and the following superoxide overproduction delay skeletal muscle regeneration through induction of overt inflammation and fibrosis in a mouse model of progressive DN.

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Su, Wen-Hong, Ching-Jen Wang, Hung-Chun Fu, Chien-Ming Sheng, Ching-Chin Tsai, Jai-Hong Cheng, and Pei-Chin Chuang. "Human Umbilical Cord Mesenchymal Stem Cells Extricate Bupivacaine-Impaired Skeletal Muscle Function via Mitigating Neutrophil-Mediated Acute Inflammation and Protecting against Fibrosis." International Journal of Molecular Sciences 20, no. 17 (September 3, 2019): 4312. http://dx.doi.org/10.3390/ijms20174312.

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Skeletal muscle injury presents a challenging traumatological dilemma, and current therapeutic options remain mediocre. This study was designed to delineate if engraftment of mesenchymal stem cells derived from umbilical cord Wharton’s jelly (uMSCs) could aid in skeletal muscle healing and persuasive molecular mechanisms. We established a skeletal muscle injury model by injection of myotoxin bupivacaine (BPVC) into quadriceps muscles of C57BL/6 mice. Post BPVC injection, neutrophils, the first host defensive line, rapidly invaded injured muscle and induced acute inflammation. Engrafted uMSCs effectively abolished neutrophil infiltration and activation, and diminished neutrophil chemotaxis, including Complement component 5a (C5a), Keratinocyte chemoattractant (KC), Macrophage inflammatory protein (MIP)-2, LPS-induced CXC chemokine (LIX), Fractalkine, Leukotriene B4 (LTB4), and Interferon-γ, as determined using a Quantibody Mouse Cytokine Array assay. Subsequently, uMSCs noticeably prevented BPVC-accelerated collagen deposition and fibrosis, measured by Masson’s trichrome staining. Remarkably, uMSCs attenuated BPVC-induced Transforming growth factor (TGF)-β1 expression, a master regulator of fibrosis. Engrafted uMSCs attenuated TGF-β1 transmitting through interrupting the canonical Sma- And Mad-Related Protein (Smad)2/3 dependent pathway and noncanonical Smad-independent Transforming growth factor beta-activated kinase (TAK)-1/p38 mitogen-activated protein kinases signaling. The uMSCs abrogated TGF-β1-induced fibrosis by reducing extracellular matrix components including fibronectin-1, collagen (COL) 1A1, and COL10A1. Most importantly, uMSCs modestly extricated BPVC-impaired gait functions, determined using CatWalk™ XT gait analysis. This work provides several innovative insights into and molecular bases for employing uMSCs to execute therapeutic potential through the elimination of neutrophil-mediated acute inflammation toward protecting against fibrosis, thereby rescuing functional impairments post injury.

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Journal articles on the topic 'Skeletal muscle fibrosis'

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