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Journal articles on the topic 'Muscle regeneration'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Kami, Katsuya, and Emiko Senba. "In Vivo Activation of STAT3 Signaling in Satellite Cells and Myofibers in Regenerating Rat Skeletal Muscles." Journal of Histochemistry & Cytochemistry 50, no. 12 (2002): 1579–89. http://dx.doi.org/10.1177/002215540205001202.

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Although growth factors and cytokines play critical roles in skeletal muscle regeneration, intracellular signaling molecules that are activated by these factors in regenerating muscles have been not elucidated. Several lines of evidence suggest that leukemia inhibitory factor (LIF) is an important cytokine for the proliferation and survival of myoblasts in vitro and acceleration of skeletal muscle regeneration. To elucidate the role of LIF signaling in regenerative responses of skeletal muscles, we examined the spatial and temporal activation patterns of an LIF-associated signaling molecule, t

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2

Gulati, Adarshk. "Pattern of skeletal muscle regeneration after reautotransplantation of regenerated muscle." Development 92, no. 1 (1986): 1–10. http://dx.doi.org/10.1242/dev.92.1.1.

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Autotransplantation of rat extensor digitorum longus muscle results in initial myofibre degeneration and subsequent regeneration from precursor myosatellite cells. To determine what effect a reinjury would have on the regenerative response, in the present,study, once transplanted and regenerated muscles were reinjured by reautotransplantion. In rats, four weeks after initial transplantation, when the regeneration was complete, the extensor digitorum longus muscle was transplanted again and the pattern of regeneration in reautotransplanted and once auto transplanted muscles was compared. Muscle

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3

Carlsen, R. C., D. Kerlin, and S. D. Gray. "Regeneration and revascularization of a nerve-intact skeletal muscle graft in the spontaneously hypertensive rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 1 (1996): R153—R161. http://dx.doi.org/10.1152/ajpregu.1996.270.1.r153.

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Skeletal muscles in hypertensive subjects develop an increased resistance to insulin that reduces their ability to incorporate glucose and synthesize glycogen. Insulin is an anabolic hormone in muscle, and muscle insulin receptors bind the growth factor, insulin-like growth factor I (IGF-I), an important contributor to muscle development and regeneration. An increase in insulin resistance in hypertensive subjects might produce muscle atrophy and weakness or limit regenerative growth after injury. Regenerative muscle growth was assessed in 24-to 26-wk-old spontaneously hypertensive rats (SHR) a

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Banerji, Christopher R. S., Don Henderson, Rabi N. Tawil, and Peter S. Zammit. "Skeletal muscle regeneration in facioscapulohumeral muscular dystrophy is correlated with pathological severity." Human Molecular Genetics 29, no. 16 (2020): 2746–60. http://dx.doi.org/10.1093/hmg/ddaa164.

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Abstract Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal-dominant myopathy characterized by slowly progressive skeletal muscle weakness and wasting. While a regenerative response is often provoked in many muscular dystrophies, little is known about whether a regenerative response is regularly elicited in FSHD muscle, prompting this study. For comparison, we also examined the similarly slowly progressing myotonic dystrophy type 2 (DM2). To first investigate regeneration at the transcriptomic level, we used the 200 human gene Hallmark Myogenesis list. This myogenesis biomarker was

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Zimowska, Małgorzata, Karolina Archacka, Edyta Brzoska, et al. "IL-4 and SDF-1 Increase Adipose Tissue-Derived Stromal Cell Ability to Improve Rat Skeletal Muscle Regeneration." International Journal of Molecular Sciences 21, no. 9 (2020): 3302. http://dx.doi.org/10.3390/ijms21093302.

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Skeletal muscle regeneration depends on the satellite cells, which, in response to injury, activate, proliferate, and reconstruct damaged tissue. However, under certain conditions, such as large injuries or myopathies, these cells might not sufficiently support repair. Thus, other cell populations, among them adipose tissue-derived stromal cells (ADSCs), are tested as a tool to improve regeneration. Importantly, the pro-regenerative action of such cells could be improved by various factors. In the current study, we tested whether IL-4 and SDF-1 could improve the ability of ADSCs to support the

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6

Dadgar, Sherry, Zuyi Wang, Helen Johnston, et al. "Asynchronous remodeling is a driver of failed regeneration in Duchenne muscular dystrophy." Journal of Cell Biology 207, no. 1 (2014): 139–58. http://dx.doi.org/10.1083/jcb.201402079.

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We sought to determine the mechanisms underlying failure of muscle regeneration that is observed in dystrophic muscle through hypothesis generation using muscle profiling data (human dystrophy and murine regeneration). We found that transforming growth factor β–centered networks strongly associated with pathological fibrosis and failed regeneration were also induced during normal regeneration but at distinct time points. We hypothesized that asynchronously regenerating microenvironments are an underlying driver of fibrosis and failed regeneration. We validated this hypothesis using an experime

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Launay, Thierry, Philippe Noirez, Gillian Butler-Browne, and Onnik Agbulut. "Expression of slow myosin heavy chain during muscle regeneration is not always dependent on muscle innervation and calcineurin phosphatase activity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 6 (2006): R1508—R1514. http://dx.doi.org/10.1152/ajpregu.00486.2005.

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In the literature, there is an ambiguity as to the respective roles played by calcineurin phosphatase activity (CPA) and muscle innervation in the reestablishment of the slow-twitch muscle phenotype after muscle regeneration in different species. In this study, we wanted to determine the role of calcineurin and muscle innervation on the appearance and maintenance of the slow phenotype during mouse muscle regeneration. The pattern of myosin expression and CPA was analyzed in adult ( n = 15), regenerating ( n = 45) and denervated-regenerating ( n = 32) slow-twitch soleus and fast-twitch extensor

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Zullo, Letizia, Matteo Bozzo, Alon Daya, et al. "The Diversity of Muscles and Their Regenerative Potential across Animals." Cells 9, no. 9 (2020): 1925. http://dx.doi.org/10.3390/cells9091925.

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Cells with contractile functions are present in almost all metazoans, and so are the related processes of muscle homeostasis and regeneration. Regeneration itself is a complex process unevenly spread across metazoans that ranges from full-body regeneration to partial reconstruction of damaged organs or body tissues, including muscles. The cellular and molecular mechanisms involved in regenerative processes can be homologous, co-opted, and/or evolved independently. By comparing the mechanisms of muscle homeostasis and regeneration throughout the diversity of animal body-plans and life cycles, i

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9

Anderson, Judy E., Laura M. McIntosh, Andrea N. Moor (neé Pernitsky), and Zipora Yablonka–Reuveni. "Levels of MyoD Protein Expression Following Injury of mdx and Normal Limb Muscle Are Modified by Thyroid Hormone." Journal of Histochemistry & Cytochemistry 46, no. 1 (1998): 59–67. http://dx.doi.org/10.1177/002215549804600108.

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Thyroid hormone (T3) affects muscle development and muscle regeneration. It also interacts with the muscle regulatory gene MyoD in culture and affects myoblast proliferation. We studied the localization of MyoD protein using a well-characterized polyclonal antibody for immunohistochemistry. Relative numbers of myogenic precursor cells per field were identified by their MyoD expression during muscle regeneration in normal and mdx dystrophic mice, with particular reference to the expression in mononuclear cells and myotubes at various T3 levels. In regeneration by normal muscles, relatively few

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10

Rahman, Fasih Ahmad, Sarah Anne Angus, Kyle Stokes, Phillip Karpowicz, and Matthew Paul Krause. "Impaired ECM Remodeling and Macrophage Activity Define Necrosis and Regeneration Following Damage in Aged Skeletal Muscle." International Journal of Molecular Sciences 21, no. 13 (2020): 4575. http://dx.doi.org/10.3390/ijms21134575.

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Regenerative capacity of skeletal muscle declines with age, the cause of which remains largely unknown. We investigated extracellular matrix (ECM) proteins and their regulators during early regeneration timepoints to define a link between aberrant ECM remodeling, and impaired aged muscle regeneration. The regeneration process was compared in young (three month old) and aged (18 month old) C56BL/6J mice at 3, 5, and 7 days following cardiotoxin-induced damage to the tibialis anterior muscle. Immunohistochemical analyses were performed to assess regenerative capacity, ECM remodeling, and the mac

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Coulton, G. R., B. Rogers, P. Strutt, M. J. Skynner, and D. J. Watt. "In situ localisation of single-stranded DNA breaks in nuclei of a subpopulation of cells within regenerating skeletal muscle of the dystrophic mdx mouse." Journal of Cell Science 102, no. 3 (1992): 653–62. http://dx.doi.org/10.1242/jcs.102.3.653.

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Degeneration of muscle fibres during the early stages of Duchenne Muscular Dystrophy (DMD) is accompanied by muscle fibre regeneration where cell division and myoblast fusion to form multinucleate myotubes within the lesions appear to recapitulate the events of normal muscle development. The mechanisms that govern the expression of genes regulating differentiation of myoblasts in regenerating skeletal muscle are of great interest for the development of future therapies designed to stimulate muscle regeneration. We show here that single-stranded breaks in DNA are localised in nuclei, using an e

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12

Pernitsky, A. N., L. M. McIntosh, and J. E. Anderson. "Hyperthyroidism impairs early repair in normal but not dystrophic mdx mouse tibialis anterior muscle. An in vivo study." Biochemistry and Cell Biology 74, no. 3 (1996): 315–24. http://dx.doi.org/10.1139/o96-034.

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The effect of hyperthyroidism on muscle repair was examined in mdx and control mice injected with triiodothyronine (T3) for 4 weeks. On day 24 of treatment, the right tibialis anterior (TA) muscle was crush-injured; 3 days later, mice received intraperitoneal [3H]thymidine to label newly synthesized DNA. One day later, muscles from both limbs were removed to study the severity of dystrophy (uncrushed muscle) and the regeneration response (crushed muscle). In uncrushed TA muscle, the area of active dystrophy (fiber damage and infiltration as a proportion of muscle cross-sectional area) was redu

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13

Zhang, Lidan, Akiyoshi Uezumi, Takayuki Kaji, et al. "Expression and Functional Analyses of Dlk1 in Muscle Stem Cells and Mesenchymal Progenitors during Muscle Regeneration." International Journal of Molecular Sciences 20, no. 13 (2019): 3269. http://dx.doi.org/10.3390/ijms20133269.

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Delta like non-canonical Notch ligand 1 (Dlk1) is a paternally expressed gene which is also known as preadipocyte factor 1 (Pref−1). The accumulation of adipocytes and expression of Dlk1 in regenerating muscle suggests a correlation between fat accumulation and Dlk1 expression in the muscle. Additionally, mice overexpressing Dlk1 show increased muscle weight, while Dlk1-null mice exhibit decreased body weight and muscle mass, indicating that Dlk1 is a critical factor in regulating skeletal muscle mass during development. The muscle regeneration process shares some features with muscle developm

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14

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 (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 mesode

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Pizza, Francis X., and Kole H. Buckley. "Regenerating Myofibers after an Acute Muscle Injury: What Do We Really Know about Them?" International Journal of Molecular Sciences 24, no. 16 (2023): 12545. http://dx.doi.org/10.3390/ijms241612545.

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Injury to skeletal muscle through trauma, physical activity, or disease initiates a process called muscle regeneration. When injured myofibers undergo necrosis, muscle regeneration gives rise to myofibers that have myonuclei in a central position, which contrasts the normal, peripheral position of myonuclei. Myofibers with central myonuclei are called regenerating myofibers and are the hallmark feature of muscle regeneration. An important and underappreciated aspect of muscle regeneration is the maturation of regenerating myofibers into a normal sized myofiber with peripheral myonuclei. Striki

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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 (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

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17

Marsh, Daniel R., David S. Criswell, James A. Carson, and Frank W. Booth. "Myogenic regulatory factors during regeneration of skeletal muscle in young, adult, and old rats." Journal of Applied Physiology 83, no. 4 (1997): 1270–75. http://dx.doi.org/10.1152/jappl.1997.83.4.1270.

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Marsh, Daniel R., David S. Criswell, James A. Carson, and Frank W. Booth. Myogenic regulatory factors during regeneration of skeletal muscle in young, adult, and old rats. J. Appl. Physiol. 83(4): 1270–1275, 1997.—Myogenic factor mRNA expression was examined during muscle regeneration after bupivacaine injection in Fischer 344/Brown Norway F1 rats aged 3, 18, and 31 mo of age (young, adult, and old, respectively). Mass of the tibialis anterior muscle in the young rats had recovered to control values by 21 days postbupivacaine injection but in adult and old rats remained 40% less than that of c

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Kohno, Shohei, Yui Yamashita, Tomoki Abe, et al. "Unloading stress disturbs muscle regeneration through perturbed recruitment and function of macrophages." Journal of Applied Physiology 112, no. 10 (2012): 1773–82. http://dx.doi.org/10.1152/japplphysiol.00103.2012.

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Skeletal muscle is one of the most sensitive tissues to mechanical loading, and unloading inhibits the regeneration potential of skeletal muscle after injury. This study was designed to elucidate the specific effects of unloading stress on the function of immunocytes during muscle regeneration after injury. We examined immunocyte infiltration and muscle regeneration in cardiotoxin (CTX)-injected soleus muscles of tail-suspended (TS) mice. In CTX-injected TS mice, the cross-sectional area of regenerating myofibers was smaller than that of weight-bearing (WB) mice, indicating that unloading dela

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Kent, Karla S., Joanne Pearce, Christine Gee, and C. K. Govind. "Regenerative fidelity in the paired claw closer muscles of lobsters." Canadian Journal of Zoology 67, no. 6 (1989): 1573–77. http://dx.doi.org/10.1139/z89-223.

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The paired claws in the lobster Homarus americanus are bilaterally asymmetric, consisting of a major (crusher) and a minor (cutter) claw. The fiber composition of the claw closer muscles is correspondingly asymmetric: the cutter muscle has predominantly fast fibers with a small ventral slow band, whereas the crusher muscle has 100% slow fibers. Loss of the paired claws results in regeneration of new ones, which resemble their predecessors in external morphology and in the fiber composition of the closer muscle. Such regenerative fidelity prevails even when the paired claws and closer muscles a

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20

Bohnert, Kathryn L., Mary K. Hastings, David R. Sinacore, et al. "Skeletal Muscle Regeneration in Advanced Diabetic Peripheral Neuropathy." Foot & Ankle International 41, no. 5 (2020): 536–48. http://dx.doi.org/10.1177/1071100720907035.

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Background: Decreased lean muscle mass in the lower extremity in diabetic peripheral neuropathy (DPN) is thought to contribute to altered joint loading, immobility, and disability. However, the mechanism behind this loss is unknown and could derive from a reduction in size of myofibers (atrophy), destruction of myofibers (degeneration), or both. Degenerative changes require participation of muscle stem (satellite) cells to regenerate lost myofibers and restore lean mass. Determining the degenerative state and residual regenerative capacity of DPN muscle will inform the utility of regeneration-

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Karra, Ravi, Matthew J. Foglia, Wen-Yee Choi, Christine Belliveau, Paige DeBenedittis, and Kenneth D. Poss. "Vegfaa instructs cardiac muscle hyperplasia in adult zebrafish." Proceedings of the National Academy of Sciences 115, no. 35 (2018): 8805–10. http://dx.doi.org/10.1073/pnas.1722594115.

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During heart development and regeneration, coronary vascularization is tightly coupled with cardiac growth. Although inhibiting vascularization causes defects in the innate regenerative response of zebrafish to heart injury, angiogenic signals are not known to be sufficient for triggering regeneration events. Here, by using a transgenic reporter strain, we found that regulatory sequences of the angiogenic factor vegfaa are active in epicardial cells of uninjured animals, as well as in epicardial and endocardial tissue adjacent to regenerating muscle upon injury. Additionally, we find that indu

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Pérez, Ruiz Ana. "A population of myogenic stem cells that survives skeletal muscle aging." Stem Cells 25, no. 4 (2007): 885–94. https://doi.org/10.5281/zenodo.14740487.

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Muscle aging is a natural process that leads to the progressive loss of muscle mass and function, impacting the quality of life, especially in older individuals. This loss is linked to a deterioration in the muscle's regenerative capacity due to the dysfunction of muscle stem cells, or satellite cells, which are essential for repairing and regenerating muscle tissue after injury or wear. As we age, the efficiency of these cells decreases, limiting the muscle's ability to regenerate properly. The main challenge of this research was to identify which populations of muscle stem cells are capable

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Church, Jarrod E., Stefan M. Gehrig, Annabel Chee, et al. "Early functional muscle regeneration after myotoxic injury in mice is unaffected by nNOS absence." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 5 (2011): R1358—R1366. http://dx.doi.org/10.1152/ajpregu.00096.2011.

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Nitric oxide (NO) is an important signaling molecule produced in skeletal muscle primarily via the neuronal subtype of NO synthase (NOS1, or nNOS). While many studies have reported NO production to be important in muscle regeneration, none have examined the contribution of nNOS-derived NO to functional muscle regeneration (i.e., restoration of the muscle's ability to produce force) after acute myotoxic injury. In the present study, we tested the hypothesis that genetic deletion of nNOS would impair functional muscle regeneration after myotoxic injury in nNOS−/− mice. We found that nNOS−/− mice

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Danieli-Betto, Daniela, Samantha Peron, Elena Germinario, et al. "Sphingosine 1-phosphate signaling is involved in skeletal muscle regeneration." American Journal of Physiology-Cell Physiology 298, no. 3 (2010): C550—C558. http://dx.doi.org/10.1152/ajpcell.00072.2009.

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Sphingosine 1-phosphate (S1P) is a bioactive lipid known to control cell growth that was recently shown to act as a trophic factor for skeletal muscle, reducing the progress of denervation atrophy. The aim of this work was to investigate whether S1P is involved in skeletal muscle fiber recovery (regeneration) after myotoxic injury induced by bupivacaine. The postnatal ability of skeletal muscle to grow and regenerate is dependent on resident stem cells called satellite cells. Immunofluorescence analysis demonstrated that S1P-specific receptors S1P1 and S1P3 are expressed by quiescent satellite

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Hosaka, Yukio, Toshifumi Yokota, Yuko Miyagoe-Suzuki та ін. "α1-Syntrophin–deficient skeletal muscle exhibits hypertrophy and aberrant formation of neuromuscular junctions during regeneration". Journal of Cell Biology 158, № 6 (2002): 1097–107. http://dx.doi.org/10.1083/jcb.200204076.

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α1-Syntrophin is a member of the family of dystrophin-associated proteins; it has been shown to recruit neuronal nitric oxide synthase and the water channel aquaporin-4 to the sarcolemma by its PSD-95/SAP-90, Discs-large, ZO-1 homologous domain. To examine the role of α1-syntrophin in muscle regeneration, we injected cardiotoxin into the tibialis anterior muscles of α1-syntrophin–null (α1syn−/−) mice. After the treatment, α1syn−/− muscles displayed remarkable hypertrophy and extensive fiber splitting compared with wild-type regenerating muscles, although the untreated muscles of the mutant mic

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Gao, Jinghui, Aria Sikal, Rachel Hankin, et al. "Extracellular Vesicles from Regenerating Skeletal Muscle Mitigate Muscle Atrophy in an Amyotrophic Lateral Sclerosis Mouse Model." Cells 14, no. 6 (2025): 464. https://doi.org/10.3390/cells14060464.

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Amyotrophic lateral sclerosis (ALS) is a devastating neuromuscular disease characterized by progressive motor neuron degeneration and muscle atrophy, with no effective treatments available. Chronic inflammation, which impairs muscle regeneration and promotes proteolysis, is a key contributor to ALS-related muscle atrophy and a promising therapeutic target. Here, we applied extracellular vesicles (EVs) derived from regenerating skeletal muscles 14 days post-acute injury (CTXD14SkM-EVs), which possess a unique anti-inflammatory profile, to target muscle defects in ALS. We found that CTXD14SkM-EV

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Kirk, S. P., M. A. Whittle, J. M. Oldham, P. M. Dobbie, and J. J. Bass. "GH regulation of the Type 2 IGF receptor in regenerating skeletal muscle of rats." Journal of Endocrinology 149, no. 1 (1996): 81–91. http://dx.doi.org/10.1677/joe.0.1490081.

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Abstract GH enhances skeletal muscle growth, and IGF-II peptide is highly expressed during regeneration. We have therefore investigated the effect of GH administration on IGF-II binding and expression in regenerating rat skeletal muscle using the techniques of receptor autoradiography and in situ hybridisation. Notexin, a myotoxin, was injected into the right M. biceps femoris (day 0), causing affected fibres to undergo necrosis followed by rapid regeneration. Animals were administered either GH (200 μg/100 g body weight) or saline vehicle daily. Contralateral muscles were used as regeneration

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Endo, Yori, Charles Hwang, Yuteng Zhang, Ronald Neppl, Shailesh Argawal, and Indranil Sinah. "AGING-RELATED VEGF IMPAIRS MUSCLE REGENERATION." Innovation in Aging 6, Supplement_1 (2022): 409. http://dx.doi.org/10.1093/geroni/igac059.1608.

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Abstract Purpose Aging is associated with frailty, a parameter that correlates with mortality and loss of muscle mass. The molecular mechanisms behind aging-associated impairment of muscle regeneration remain incompletely understood. We hypothesized VEGF-A with known role in angiogenesis and muscle progenitor differentiation to regulate regeneration in aged skeletal muscle. Methods Young C57BL/6 (10 weeks old) and old C57BL/6 mice (24 months old) were subjected to muscle cryoinjury to induce regeneration. Quantifications of cross-sectional area (CSA) of regenerating myofibers were performed. T

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Hara, Mie, Shinsuke Yuasa, Kenichiro Shimoji, et al. "G-CSF influences mouse skeletal muscle development and regeneration by stimulating myoblast proliferation." Journal of Experimental Medicine 208, no. 4 (2011): 715–27. http://dx.doi.org/10.1084/jem.20101059.

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After skeletal muscle injury, neutrophils, monocytes, and macrophages infiltrate the damaged area; this is followed by rapid proliferation of myoblasts derived from muscle stem cells (also called satellite cells). Although it is known that inflammation triggers skeletal muscle regeneration, the underlying molecular mechanisms remain incompletely understood. In this study, we show that granulocyte colony-stimulating factor (G-CSF) receptor (G-CSFR) is expressed in developing somites. G-CSFR and G-CSF were expressed in myoblasts of mouse embryos during the midgestational stage but not in mature

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Contreras-Shannon, Verónica, Oscar Ochoa, Sara M. Reyes-Reyna, et al. "Fat accumulation with altered inflammation and regeneration in skeletal muscle of CCR2−/− mice following ischemic injury." American Journal of Physiology-Cell Physiology 292, no. 2 (2007): C953—C967. http://dx.doi.org/10.1152/ajpcell.00154.2006.

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Chemokines recruit inflammatory cells to sites of injury, but the role of the CC chemokine receptor 2 (CCR2) during regenerative processes following ischemia is poorly understood. We studied injury, inflammation, perfusion, capillary formation, monocyte chemotactic protein-1 (MCP-1) levels, muscle regeneration, fat accumulation, and transcription factor activation in hindlimb muscles of CCR2−/− and wild-type (WT) mice following femoral artery excision (FAE). In both groups, muscle injury and restoration of vascular perfusion were similar. Nevertheless, edema and neutrophil accumulation were si

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Oikawa, Satoshi, Minjung Lee, and Takayuki Akimoto. "Conditional Deletion of Dicer in Adult Mice Impairs Skeletal Muscle Regeneration." International Journal of Molecular Sciences 20, no. 22 (2019): 5686. http://dx.doi.org/10.3390/ijms20225686.

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Skeletal muscle has a remarkable regenerative capacity, which is orchestrated by multiple processes, including the proliferation, fusion, and differentiation of the resident stem cells in muscle. MicroRNAs (miRNAs) are small noncoding RNAs that mediate the translational repression or degradation of mRNA to regulate diverse biological functions. Previous studies have suggested that several miRNAs play important roles in myoblast proliferation and differentiation in vitro. However, their potential roles in skeletal muscle regeneration in vivo have not been fully established. In this study, we ge

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Morawin, Barbara, and Agnieszka Zembroń-Łacny. "Role of endocrine factors and stem cells in skeletal muscle regeneration." Postępy Higieny i Medycyny Doświadczalnej 75 (June 2, 2021): 371–84. http://dx.doi.org/10.5604/01.3001.0014.9125.

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The process of reconstructing damaged skeletal muscles involves degeneration, inflammatory and immune responses, regeneration and reorganization, which are regulated by a number of immune-endocrine factors affecting muscle cells and satellite cells (SCs). One of these molecules is testosterone (T), which binds to the androgen receptor (AR) to initiate the expression of the muscle isoform of insulin-like growth factor 1 (IGF-1Ec). The interaction between T and IGF-1Ec stimulates the growth and regeneration of skeletal muscles by inhibiting apoptosis, enhancement of SCs proliferation and myoblas

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Stupka, Nicole, Jonathan D. Schertzer, Rhonda Bassel-Duby, Eric N. Olson та Gordon S. Lynch. "Calcineurin-Aα activation enhances the structure and function of regenerating muscles after myotoxic injury". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, № 2 (2007): R686—R694. http://dx.doi.org/10.1152/ajpregu.00612.2006.

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Calcineurin signaling is essential for successful muscle regeneration. Although calcineurin inhibition compromises muscle repair, it is not known whether calcineurin activation can enhance muscle repair after injury. Tibialis anterior (TA) muscles from adult wild-type (WT) and transgenic mice overexpressing the constitutively active calcineurin-Aα transgene under the control of the mitochondrial creatine kinase promoter (MCK-CnAα*) were injected with the myotoxic snake venom Notexin to destroy all muscle fibers. The TA muscle of the contralateral limb served as the uninjured control. Muscle st

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Takagi, Ryo, Naoto Fujita, Takamitsu Arakawa, Shigeo Kawada, Naokata Ishii, and Akinori Miki. "Influence of icing on muscle regeneration after crush injury to skeletal muscles in rats." Journal of Applied Physiology 110, no. 2 (2011): 382–88. http://dx.doi.org/10.1152/japplphysiol.01187.2010.

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The influence of icing on muscle regeneration after crush injury was examined in the rat extensor digitorum longus. After the injury, animals were randomly divided into nonicing and icing groups. In the latter, ice packs were applied for 20 min. Due to the icing, degeneration of the necrotic muscle fibers and differentiation of satellite cells at early stages of regeneration were retarded by ∼1 day. In the icing group, the ratio of regenerating fibers showing central nucleus at 14 days after the injury was higher, and cross-sectional area of the muscle fibers at 28 days was evidently smaller t

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Kuang, Shihuan, Feng Yue, and Stephanie Oprescu. "193 Single Cell RNA-sequencing Reveals a Role of Lipid Metabolism in Muscle Satellite Cells." Journal of Animal Science 99, Supplement_3 (2021): 104–5. http://dx.doi.org/10.1093/jas/skab235.189.

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Abstract Single Cell RNA-sequencing (scRNA-seq) is a powerful technique to deconvolute gene expression of various subset of cells intermingled within a complex tissue, such as the skeletal muscle. We first used scRNA-seq to understand dynamics of cell populations and their gene expression during muscle regeneration in murine limb muscles. This leads to the identification of a subset of satellite cells (the resident stem cells of skeletal muscles) with immune gene signatures in regenerating muscles. Next, we used scRNA-seq to examine gene expression dynamics of satellite cells at various status

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Clow, Charlene, and Bernard J. Jasmin. "Brain-derived Neurotrophic Factor Regulates Satellite Cell Differentiation and Skeltal Muscle Regeneration." Molecular Biology of the Cell 21, no. 13 (2010): 2182–90. http://dx.doi.org/10.1091/mbc.e10-02-0154.

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In adult skeletal muscle, brain-derived neurotrophic factor (BDNF) is expressed in myogenic progenitors known as satellite cells. To functionally address the role of BDNF in muscle satellite cells and regeneration in vivo, we generated a mouse in which BDNF is specifically depleted from skeletal muscle cells. For comparative purposes, and to determine the specific role of muscle-derived BDNF, we also examined muscles of the complete BDNF−/− mouse. In both models, expression of the satellite cell marker Pax7 was significantly decreased. Furthermore, proliferation and differentiation of primary

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Brenner, H. R., A. Herczeg, and C. R. Slater. "Synapse-specific expression of acetylcholine receptor genes and their products at original synaptic sites in rat soleus muscle fibres regenerating in the absence of innervation." Development 116, no. 1 (1992): 41–53. http://dx.doi.org/10.1242/dev.116.1.41.

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To test the hypothesis that synaptic basal lamina can induce synapse-specific expression of acetylcholine receptor (AChR) genes, we examined the levels mRNA for the alpha- and epsilon-subunits of the AChR in regenerating rat soleus muscles up to 17 days of regeneration. Following destruction of all muscle fibres and their nuclei by exposure to venom of the Australian tiger snake, new fibres regenerated within the original basal lamina sheaths. Northern blots showed that original mRNA was lost during degeneration. Early in regeneration, both alpha- and epsilon-subunit mRNAs were present through

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Hirano, Kotaro, Masaki Tsuchiya, Akifumi Shiomi, et al. "The mechanosensitive ion channel PIEZO1 promotes satellite cell function in muscle regeneration." Life Science Alliance 6, no. 2 (2022): e202201783. http://dx.doi.org/10.26508/lsa.202201783.

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Muscle satellite cells (MuSCs), myogenic stem cells in skeletal muscles, play an essential role in muscle regeneration. After skeletal muscle injury, quiescent MuSCs are activated to enter the cell cycle and proliferate, thereby initiating regeneration; however, the mechanisms that ensure successful MuSC division, including chromosome segregation, remain unclear. Here, we show that PIEZO1, a calcium ion (Ca2+)-permeable cation channel activated by membrane tension, mediates spontaneous Ca2+influx to control the regenerative function of MuSCs. Our genetic engineering approach in mice revealed t

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Liu, Juan, Dominik Saul, Kai Oliver Böker, Jennifer Ernst, Wolfgang Lehman, and Arndt F. Schilling. "Current Methods for Skeletal Muscle Tissue Repair and Regeneration." BioMed Research International 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/1984879.

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Skeletal muscle has the capacity of regeneration after injury. However, for large volumes of muscle loss, this regeneration needs interventional support. Consequently, muscle injury provides an ongoing reconstructive and regenerative challenge in clinical work. To promote muscle repair and regeneration, different strategies have been developed within the last century and especially during the last few decades, including surgical techniques, physical therapy, biomaterials, and muscular tissue engineering as well as cell therapy. Still, there is a great need to develop new methods and materials,

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Slack, J. M. W., C. W. Beck, C. Gargioli, and B. Christen. "Cellular and molecular mechanisms of regeneration in Xenopus." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, no. 1445 (2004): 745–51. http://dx.doi.org/10.1098/rstb.2004.1463.

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We have employed transgenic methods combined with embryonic grafting to analyse the mechanisms of regeneration in Xenopus tadpoles. The Xenopus tadpole tail contains a spinal cord, notochord and segmented muscles, and all tissues are replaced when the tail regenerates after amputation. We show that there is a refractory period of very low regenerative ability in the early tadpole stage. Tracing of cell lineage with the use of single tissue transgenic grafts labelled with green fluorescent protein (GFP) shows that there is no de-differentiation and no metaplasia during regeneration. The spinal

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Ge, Yejing, Ai-Luen Wu, Christine Warnes, et al. "mTOR regulates skeletal muscle regeneration in vivo through kinase-dependent and kinase-independent mechanisms." American Journal of Physiology-Cell Physiology 297, no. 6 (2009): C1434—C1444. http://dx.doi.org/10.1152/ajpcell.00248.2009.

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Rapamycin-sensitive signaling is required for skeletal muscle differentiation and remodeling. In cultured myoblasts, the mammalian target of rapamycin (mTOR) has been reported to regulate differentiation at different stages through distinct mechanisms, including one that is independent of mTOR kinase activity. However, the kinase-independent function of mTOR remains controversial, and no in vivo studies have examined those mTOR myogenic mechanisms previously identified in vitro. In this study, we find that rapamycin impairs injury-induced muscle regeneration. To validate the role of mTOR with

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Barton, Elisabeth R., Linda Morris, Antonio Musaro, Nadia Rosenthal, and H. Lee Sweeney. "Muscle-specific expression of insulin-like growth factor I counters muscle decline in mdx mice." Journal of Cell Biology 157, no. 1 (2002): 137–48. http://dx.doi.org/10.1083/jcb.200108071.

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Duchenne muscular dystrophy is an X-linked degenerative disorder of muscle caused by the absence of the protein dystrophin. A major consequence of muscular dystrophy is that the normal regenerative capacity of skeletal muscle cannot compensate for increased susceptibility to damage, leading to repetitive cycles of degeneration–regeneration and ultimately resulting in the replacement of muscle fibers with fibrotic tissue. Because insulin-like growth factor I (IGF-I) has been shown to enhance muscle regeneration and protein synthetic pathways, we asked whether high levels of muscle-specific expr

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Liu, Qi, Su Pan, Shijie Liu, et al. "Suppressing Hippo signaling in the stem cell niche promotes skeletal muscle regeneration." Stem Cells 39, no. 6 (2021): 737–49. http://dx.doi.org/10.1002/stem.3343.

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Abstract Lack of blood flow to the lower extremities in peripheral arterial disease causes oxygen and nutrient deprivation in ischemic skeletal muscles, leading to functional impairment. Treatment options for muscle regeneration in this scenario are lacking. Here, we selectively targeted the Hippo pathway in myofibers, which provide architectural support for muscle stem cell niches, to facilitate functional muscle recovery in ischemic extremities by promoting angiogenesis, neovascularization, and myogenesis. We knocked down the core Hippo pathway component, Salvador (SAV1), by using an adeno-a

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Ribchester, R. R. "Co‐existence and elimination of convergent motor nerve terminals in reinnervated and paralysed adult rat skeletal muscle." Journal of Physiology 466, no. 1 (1993): 421–41. http://dx.doi.org/10.1113/jphysiol.1993.sp019728.

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1. Experiments were carried out to determine whether neuromuscular synapse elimination can occur in skeletal muscle in the complete absence of conducted neural activity, using reinnervation of partially denervated adult muscle as a paradigm. Partially denervated rat lumbrical muscles were paralysed with a nerve conduction block applied to the sciatic nerve during regeneration of injured sural nerve motor axons. Both intact (lateral plantar nerve) and regenerating motor axons converging on the same muscle fibres were therefore inactive. 2. Paralysed muscles expressed prolonged twitch contractio

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Rebalka, Irena A., Cynthia M. F. Monaco, Nina E. Varah, et al. "Loss of the adipokine lipocalin-2 impairs satellite cell activation and skeletal muscle regeneration." American Journal of Physiology-Cell Physiology 315, no. 5 (2018): C714—C721. http://dx.doi.org/10.1152/ajpcell.00195.2017.

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Lipocalin-2 (LCN2) is an adipokine previously described for its contribution to numerous processes, including innate immunity and energy metabolism. LCN2 has also been demonstrated to be an extracellular matrix (ECM) regulator through its association with the ECM protease matrix metalloproteinase-9 (MMP-9). With the global rise in obesity and the associated comorbidities related to increasing adiposity, it is imperative to gain an understanding of the cross talk between adipose tissue and other metabolic tissues, such as skeletal muscle. Given the function of LCN2 on the ECM in other tissues a

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Grabowska, Iwona, Malgorzata Zimowska, Karolina Maciejewska, et al. "Adipose Tissue-Derived Stromal Cells in Matrigel Impact the Regeneration of Severely Damaged Skeletal Muscles." International Journal of Molecular Sciences 20, no. 13 (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 ADSC

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Milewska, Marta, and Katarzyna Grzelkowska-Kowalczyk. "Role of proinflammatory cytokines and growth factors in skeletal muscle regeneration." Medycyna Weterynaryjna 72, no. 8 (2016): 472–78. http://dx.doi.org/10.21521/mw.5551.

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Skeletal muscle healing after injury can be divided into three distinct but overlapping phases. The destruction phase is characterized by rupture followed by necrosis of muscle fibers, formation of hematoma and inflammatory reaction. During the repair phase a necrotic tissue is phagocyted by macrophages, muscle fibers are regenerating and connective tissue scars are formed. The remodeling phase concerns the period when regenerating muscle fibers mature, scar contraction and reorganization occurs and the muscle recovers its functional efficiency. Proinflammatory cytokines (IL-1β, IL-6, IL-8, TN

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Bondesen, Brenda A., Stephen T. Mills, Kristy M. Kegley, and Grace K. Pavlath. "The COX-2 pathway is essential during early stages of skeletal muscle regeneration." American Journal of Physiology-Cell Physiology 287, no. 2 (2004): C475—C483. http://dx.doi.org/10.1152/ajpcell.00088.2004.

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Skeletal muscle regeneration comprises several overlapping cellular processes, including inflammation and myogenesis. Prostaglandins (PGs) may regulate muscle regeneration, because they modulate inflammation and are involved in various stages of myogenesis in vitro. PG synthesis is catalyzed by different isoforms of cyclooxygenase (COX), which are inhibited by nonsteroidal anti-inflammatory drugs. Although experiments employing nonsteroidal anti-inflammatory drugs have implicated PGs in tissue repair, how PGs regulate muscle regeneration remains unclear, and the potentially distinct roles of d

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CIECIERSKA, ANNA, TOMASZ SADKOWSKI, and TOMASZ MOTYL. "Role of satellite cells in growth and regeneration of skeletal muscles." Medycyna Weterynaryjna 75, no. 11 (2019): 6349–2019. http://dx.doi.org/10.21521/mw.6349.

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Postnatal growth and regeneration capacity of skeletal muscles is dependent mainly on adult muscle stem cells called satellite cells. Satellite cells are quiescent mononucleated cells that are normally located outside the sarcolemma within the basal lamina of the muscle fiber. Their activation, which results from injury, is manifested by mobilization, proliferation, differentiation and, ultimately, fusion into new muscle fibers. The satellite cell pool is responsible for the remarkable regenerative capacity of skeletal muscles. Moreover, these cells are capable of self-renewal and can give ris

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Pereira, T., P. A. S. Armada-da Silva, I. Amorim, et al. "Effects of Human Mesenchymal Stem Cells Isolated from Wharton’s Jelly of the Umbilical Cord and Conditioned Media on Skeletal Muscle Regeneration Using a Myectomy Model." Stem Cells International 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/376918.

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Skeletal muscle has good regenerative capacity, but the extent of muscle injury and the developed fibrosis might prevent complete regeneration. Thein vivoapplication of human mesenchymal stem cells (HMSCs) of the umbilical cord and the conditioned media (CM) where the HMSCs were cultured and expanded, associated with different vehicles to induce muscle regeneration, was evaluated in a rat myectomy model. Two commercially available vehicles and a spherical hydrogel developed by our research group were used. The treated groups obtained interesting results in terms of muscle regeneration, both in

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