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FEBS Journal

Cover image for Vol. 280 Issue 17

Special Issue: Myogenesis

September 2013

Volume 280, Issue 17

Pages i–iii, 3979–4336

  1. Front Cover

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Introduction
    5. Mechanisms of Myogenesis
    6. Satellite Cells and Muscle Stem Cells
    7. Muscle Fibrosis and Inflammation
    8. Muscular Dystrophy
    9. Stem Cell Therapy
    10. Neuromuscular and Muscle Diseases
    11. Author index
    12. Table of Contents
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      Front Cover (page i)

      Article first published online: 20 AUG 2013 | DOI: 10.1111/j.1742-4658.2013.08792.x

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      Muscle resident stem cells with potential myogenic activity (by R-H Zhang in Judson et al., pp. 4090-4098) with crystal structure of myostatin/follistatin complex (PDB entry 3hh2).

  2. Editorial Information

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Introduction
    5. Mechanisms of Myogenesis
    6. Satellite Cells and Muscle Stem Cells
    7. Muscle Fibrosis and Inflammation
    8. Muscular Dystrophy
    9. Stem Cell Therapy
    10. Neuromuscular and Muscle Diseases
    11. Author index
    12. Table of Contents
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      Editorial Information (pages ii–iii)

      Article first published online: 20 AUG 2013 | DOI: 10.1111/j.1742-4658.2013.08792_1.x

  3. Introduction

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Introduction
    5. Mechanisms of Myogenesis
    6. Satellite Cells and Muscle Stem Cells
    7. Muscle Fibrosis and Inflammation
    8. Muscular Dystrophy
    9. Stem Cell Therapy
    10. Neuromuscular and Muscle Diseases
    11. Author index
    12. Table of Contents
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      Special Issue: Myogenesis : Introduction (page 3979)

      Pura Muñoz-Cánoves and Daniel Michele

      Article first published online: 14 AUG 2013 | DOI: 10.1111/febs.12454

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      Research on myogenesis, the process of formation of skeletal muscle, advances knowledge of the biology of this tissue from a cellular and molecular perspective, and greatly contributes to the better understanding of tissue-specific stem cell functions and regeneration. New insights into stem cell functioning, advanced methodological approaches and new emerging therapeutic alternatives for severe muscle pathologies were discussed at two conferences on skeletal muscle held in 2012: ‘Frontiers in Myogenesis: Development, Function and Repair of the Muscle Cell’, in New York, and ‘New Directions in Biology and Disease of Skeletal Muscle,’ in New Orleans.

  4. Mechanisms of Myogenesis

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Introduction
    5. Mechanisms of Myogenesis
    6. Satellite Cells and Muscle Stem Cells
    7. Muscle Fibrosis and Inflammation
    8. Muscular Dystrophy
    9. Stem Cell Therapy
    10. Neuromuscular and Muscle Diseases
    11. Author index
    12. Table of Contents
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      Dial M(RF) for myogenesis (pages 3980–3990)

      Natalia Moncaut, Peter W. J. Rigby and Jaime J. Carvajal

      Article first published online: 5 JUL 2013 | DOI: 10.1111/febs.12379

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      The transcriptional regulatory network that controls the determination and differentiation of skeletal muscle cells has at its core the four myogenic regulatory factors (MRFs): Myf5, MyoD, Mrf4 and MyoG. The application of new genome-wide approaches, including the identification and functional analyses of miRNA regulation, is providing important information as to how the MRFs function to activate the terminal differentiation programme.

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      Differential modulation of cell cycle progression distinguishes members of the myogenic regulatory factor family of transcription factors (pages 3991–4003)

      Kulwant Singh and F. Jeffrey Dilworth

      Article first published online: 8 MAR 2013 | DOI: 10.1111/febs.12188

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      Myogenic regulatory factors (MRFs - MyoD, Myf5, Myogenin, and MRF4) are key transcription factors that regulate gene expression that establish the skeletal muscle cell fate. Here, we discuss the current literature concerning the role of MRFs in modulating cell cycle progression, and define Myogenin expression as a “point of no return” for establishing permanent cell cycle exit during muscle differentiation.

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      Metabolic reprogramming as a novel regulator of skeletal muscle development and regeneration (pages 4004–4013)

      James G. Ryall

      Article first published online: 8 MAR 2013 | DOI: 10.1111/febs.12189

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      Adult skeletal muscle stem cells, termed satellite cells, are known to co-localize with blood vessels, indicating that satellite cell function may be linked to changes in the local metabolism. Here, the metabolic reprogramming of satellite cells during activation, specification, proliferation and differentiation is discussed, with reference to recent findings in other stem cell populations and tumor cells.

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      Epigenetic control of skeletal muscle regeneration : Integrating genetic determinants and environmental changes (pages 4014–4025)

      Lorenzo Giordani and Pier Lorenzo Puri

      Article first published online: 15 JUL 2013 | DOI: 10.1111/febs.12383

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      Recent evidence has revealed that discrete populations of adult cells can retain the ability to adopt alternative cell fates in response to environmental cues. The molecular determinants of these transitions reveal how dynamic chromatin states can generate flexible epigenetic landscapes that confer the ability to retain partial pluripotency and adapt to environmental changes.

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      Development of the diaphragm – a skeletal muscle essential for mammalian respiration (pages 4026–4035)

      Allyson J. Merrell and Gabrielle Kardon

      Article first published online: 7 MAY 2013 | DOI: 10.1111/febs.12274

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      The mammalian diaphragm is a critical skeletal muscle essential for respiration. Defects in diaphragm development, leading to congenital diaphragmatic hernias (CDH), are common and often lethal birth defects. Thus, an understanding of diaphragm development normally and during herniation is important. We review the current knowledge of the diaphragm's embryological origins and morphogenesis and the genetic and developmental etiology of CDH.

  5. Satellite Cells and Muscle Stem Cells

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Introduction
    5. Mechanisms of Myogenesis
    6. Satellite Cells and Muscle Stem Cells
    7. Muscle Fibrosis and Inflammation
    8. Muscular Dystrophy
    9. Stem Cell Therapy
    10. Neuromuscular and Muscle Diseases
    11. Author index
    12. Table of Contents
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      Lying low but ready for action: the quiescent muscle satellite cell (pages 4036–4050)

      Didier Montarras, Aurore L'honoré and Margaret Buckingham

      Article first published online: 12 JUL 2013 | DOI: 10.1111/febs.12372

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      In this review, we present the quiescent satellite cell in its niche on the muscle fibre. We discuss its environment and how this myogenic stem cell protects itself and maintains its quiescent state, while remaining ready for rapid activation and regeneration of skeletal muscle in response to external signals.

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      Functional dysregulation of stem cells during aging: a focus on skeletal muscle stem cells (pages 4051–4062)

      Laura García-Prat, Pedro Sousa-Victor and Pura Muñoz-Cánoves

      Article first published online: 21 MAR 2013 | DOI: 10.1111/febs.12221

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      Skeletal muscle relies on adult stem cells (satellite cells) to regenerate and this capacity declines with aging. Aged satellite cells improve their regenerative potential when exposed to a youthful environment. We review the literature on the coordinated relationship between extrinsic and intrinsic factors regulating satellite cells functions, which in turn determine tissue homeostasis and repair during aging.

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      Moderate-intensity treadmill running promotes expansion of the satellite cell pool in young and old mice (pages 4063–4073)

      Gabi Shefer, Gat Rauner, Pascal Stuelsatz, Dafna Benayahu and Zipora Yablonka-Reuveni

      Article first published online: 12 APR 2013 | DOI: 10.1111/febs.12228

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      Satellite cells (SCs) are myogenic progenitors essential for skeletal muscle repair. Here, we show that moderate-intensity treadmill running is associated with an increase in SC numbers in young and old mice. This experimental setting establishes a paradigm for investigating mechanisms that control the expansion of SCs at their native niche by the myofiber and SC role in muscle aging.

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      A myogenic precursor cell that could contribute to regeneration in zebrafish and its similarity to the satellite cell (pages 4074–4088)

      Ashley L. Siegel, David B. Gurevich and Peter D. Currie

      Article first published online: 24 MAY 2013 | DOI: 10.1111/febs.12300

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      Mammalian muscle regeneration occurs through a specialized self-renewing stem cell, the satellite cell. How broadly deployed this is within the vertebrate phylogeny remains an open question. In this review, we examine the evidence for or against broad phylogenetic distribution of satellite cells. We conclude that, in vertebrates examined an analogous cell to the satellite cells is deployed in muscle regeneration.

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      Enter the matrix: shape, signal and superhighway (pages 4089–4099)

      Dane K. Lund and D. D. W. Cornelison

      Article first published online: 1 MAR 2013 | DOI: 10.1111/febs.12171

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      The extracellular matrix of skeletal muscle is a highly ordered and regulated series of structures that participate in biophysical and biochemical interactions with local cell types, including muscle stem cells (satellite cells). We provide an overview of these interactions in the context of muscle homeostasis and repair, highlight significant unanswered question, and suggest areas of future interest.

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      Tissue-resident mesenchymal stem/progenitor cells in skeletal muscle: collaborators or saboteurs? (pages 4100–4108)

      Robert N. Judson, Regan-Heng Zhang and Fabio M. A. Rossi

      Article first published online: 24 JUN 2013 | DOI: 10.1111/febs.12370

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      Like most postnatal tissues, skeletal muscle plays host to a heterogeneous pool of tissue resident mesenchymal stem/progenitor cells. These progenitors play critical supporting roles in regeneration, collaborating with the host stem cell pool (satellite cells) to ensure effective repair. In disease, however, mesenchymal stem/progenitor cells adopt a more sinister role, sabotaging regeneration and providing a major source of fibrosis in dystrophic muscle.

  6. Muscle Fibrosis and Inflammation

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Introduction
    5. Mechanisms of Myogenesis
    6. Satellite Cells and Muscle Stem Cells
    7. Muscle Fibrosis and Inflammation
    8. Muscular Dystrophy
    9. Stem Cell Therapy
    10. Neuromuscular and Muscle Diseases
    11. Author index
    12. Table of Contents
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      Role of proteoglycans in the regulation of the skeletal muscle fibrotic response (pages 4109–4117)

      Enrique Brandan and Jaime Gutierrez

      Article first published online: 2 MAY 2013 | DOI: 10.1111/febs.12278

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      Myogenesis consists of a highly organized and regulated sequence of cellular processes with the aim of forming or repairing muscle tissue. Proteoglycans modulate factors responsible for the fibrotic response associated with skeletal muscular dystrophies. Transforming growth factor-β and connective tissue growth factor have gained great attention as factors participating in the fibrotic response in skeletal muscle.

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      Monocyte/macrophage interactions with myogenic precursor cells during skeletal muscle regeneration (pages 4118–4130)

      Marielle Saclier, Sylvain Cuvellier, Mélanie Magnan, Rémi Mounier and Bénédicte Chazaud

      Article first published online: 28 FEB 2013 | DOI: 10.1111/febs.12166

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      Skeletal muscle regenerates after injury thanks to myogenic precursor cells. Macrophages are continuously present during muscle regeneration. While in resting muscle, macrophages are located in the epimysium, they infiltrate the parenchyma after muscle injury. A sequence of pro-inflammatory then anti-inflammatory macrophages accompanies muscle regeneration, each subset of macrophages providing specific cues to myogenic cells for proliferation then differentiation.

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      Interleukin-6 myokine signaling in skeletal muscle: a double-edged sword? (pages 4131–4148)

      Pura Muñoz-Cánoves, Camilla Scheele, Bente K. Pedersen and Antonio L. Serrano

      Article first published online: 18 JUN 2013 | DOI: 10.1111/febs.12338

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      IL-6 is a cytokine with pleiotropic functions. Skeletal muscle produces and releases IL-6 after prolonged exercise and is considered a myokine. IL-6 signaling stimulates hypertrophic muscle growth and de novo myogenesis. However, IL-6 also promotes atrophy and muscle wasting. We review the current evidence for these apparently contradictory effects, the mechanisms involved and discuss their possible biological implications.

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      Oxidative stress and pathology in muscular dystrophies: focus on protein thiol oxidation and dysferlinopathies (pages 4149–4164)

      Jessica R. Terrill, Hannah G. Radley-Crabb, Tomohito Iwasaki, Frances A. Lemckert, Peter G. Arthur and Miranda D. Grounds

      Article first published online: 15 FEB 2013 | DOI: 10.1111/febs.12142

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      Disturbed levels of reactive oxygen species are believed to contribute to the pathology of many muscular dystrophies. New data are presented that show significantly increased protein thiol oxidation and high levels of lipofuscin (a measure of cumulative oxidative damage) in dysferlin-deficient muscles of A/J mice at various ages. The significance of this is critically compared with dystrophin-deficient mdx mice.

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      Dysferlin-deficient muscular dystrophy and innate immune activation (pages 4165–4176)

      Andrew Mariano, Audrey Henning and Renzhi Han

      Article first published online: 22 APR 2013 | DOI: 10.1111/febs.12261

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      Failure to repair plasma membrane disruption leads to individual cell death, which may also produce systemic influence by triggering sterile immunological responses. In this review, we discuss recent progress on understanding the mechanisms underlying muscle cell membrane repair and the potential mediators of innate immune activation when membrane repair system is defective, specifically focusing on pathology associated with dysferlin deficiency.

  7. Muscular Dystrophy

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Introduction
    5. Mechanisms of Myogenesis
    6. Satellite Cells and Muscle Stem Cells
    7. Muscle Fibrosis and Inflammation
    8. Muscular Dystrophy
    9. Stem Cell Therapy
    10. Neuromuscular and Muscle Diseases
    11. Author index
    12. Table of Contents
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      The mdx mouse model as a surrogate for Duchenne muscular dystrophy (pages 4177–4186)

      Terence A. Partridge

      Article first published online: 22 APR 2013 | DOI: 10.1111/febs.12267

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      The mdx mouse is heavily used as a model of Duchenne muscular dystrophy. In order to make the best use of it, we need to understand in what ways it is similar and in what ways it is different. Most important are the differences in size and in the mode of growth.

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      Swimming into prominence: the zebrafish as a valuable tool for studying human myopathies and muscular dystrophies (pages 4187–4197)

      Elizabeth M. Gibbs, Eric J. Horstick and James J. Dowling

      Article first published online: 25 JUL 2013 | DOI: 10.1111/febs.12412

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      Zebrafish models of muscular dystrophies and myopathies recapitulate the major features of the corresponding human disorders, and have proven exceptionally useful for elucidating pathogenic mechanisms and identifying novel molecular therapies. In this review, we describe the features that make zebrafish an ideal system for studying muscle disease, and highlight key contributions they have made to our understanding of muscle disorders.

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      Modifying muscular dystrophy through transforming growth factor-β (pages 4198–4209)

      Ermelinda Ceco and Elizabeth M. McNally

      Article first published online: 24 APR 2013 | DOI: 10.1111/febs.12266

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      Genetic data from humans and mouse models supports that modifier genes can alter the outcome in muscular dystrophy. Recent data points to the TGF-β pathway as an important modifier useful for prognosis and for therapeutic intervention in muscular dystrophy. TGF-β works through extracellular and intracellular pathways to regulate fibrosis and muscle function.

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      The potential of sarcospan in adhesion complex replacement therapeutics for the treatment of muscular dystrophy (pages 4210–4229)

      Jamie L. Marshall, Yukwah Kwok, Brian J. McMorran, Linda G. Baum and Rachelle H. Crosbie-Watson

      Article first published online: 13 MAY 2013 | DOI: 10.1111/febs.12295

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      Sarcospan facilitates interactions between the adhesion glycoprotein complexes, dystrophin- and utrophin-glycoprotein complexes and α7β1 integrin, which protect the sarcolemma during muscle contraction. Over-expression of sarcospan ameliorates dystrophic pathology in mdx muscle by upregulating integrins and the utrophin-glycoprotein complex, Akt phosphorylation, and glycosylation of the dystroglycans. These mechanisms result in stabilization of the sarcolemmal membrane by restoring connections to laminin.

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      PABPN1: molecular function and muscle disease (pages 4230–4250)

      Ayan Banerjee, Luciano H. Apponi, Grace K. Pavlath and Anita H. Corbett

      Article first published online: 24 MAY 2013 | DOI: 10.1111/febs.12294

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      The polyadenylate-binding nuclear protein 1 (PABPN1) plays a critical role in gene expression. Although PABPN1 is ubiquitously expressed, a mutation in the PABPN1 gene causes a muscle-specific disease, oculopharyngeal muscular dystrophy (OPMD). This review addresses both the molecular functions of PABPN1 and the approaches being used to elucidate the mechanisms underlying the muscle-specific pathogenesis of OPMD.

  8. Stem Cell Therapy

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Introduction
    5. Mechanisms of Myogenesis
    6. Satellite Cells and Muscle Stem Cells
    7. Muscle Fibrosis and Inflammation
    8. Muscular Dystrophy
    9. Stem Cell Therapy
    10. Neuromuscular and Muscle Diseases
    11. Author index
    12. Table of Contents
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      Perspectives of stem cell therapy in Duchenne muscular dystrophy (pages 4251–4262)

      Mirella Meregalli, Andrea Farini, Marzia Belicchi, Daniele Parolini, Letizia Cassinelli, Paola Razini, Clementina Sitzia and Yvan Torrente

      Article first published online: 7 JAN 2013 | DOI: 10.1111/febs.12083

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      Duchenne muscular dystrophy (DMD) is the most common form of muscular dystrophy and unfortunately no effective therapy is available at present. As stem cells received much attention for their potential use in cell-based therapies for human diseases, herein we described multiple types of resident and circulating myogenic stem cells, their characterization and their possible use to treat muscular dystrophies.

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      Repair or replace? Exploiting novel gene and cell therapy strategies for muscular dystrophies (pages 4263–4280)

      Sara Benedetti, Hidetoshi Hoshiya and Francesco Saverio Tedesco

      Article first published online: 4 MAR 2013 | DOI: 10.1111/febs.12178

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      Muscular dystrophies are severe genetic disorders characterized by muscle wasting. Although there is no effective therapy, different experimental strategies have been developed. Here, we highlight recent experimental therapies based upon gene replacement and gene/expression repair, including exon-skipping, vector-mediated gene therapy and cell therapy. Different forms of muscular dystrophy will be discussed, with an emphasis on Duchenne muscular dystrophy.

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      Recent progress in satellite cell/myoblast engraftment – relevance for therapy (pages 4281–4293)

      Deborah Briggs and Jennifer E. Morgan

      Article first published online: 24 APR 2013 | DOI: 10.1111/febs.12273

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      There is currently no cure for muscular dystrophies, although several promising strategies are under investigation. One such strategy is transplantation of satellite cells, or their myoblast progeny, to repair and regenerate muscle fibres and repopulate the stem cell niche. We review recent advances in satellite cell/myoblast therapy and discuss the challenges that remain for it to become a realistic therapy.

  9. Neuromuscular and Muscle Diseases

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Introduction
    5. Mechanisms of Myogenesis
    6. Satellite Cells and Muscle Stem Cells
    7. Muscle Fibrosis and Inflammation
    8. Muscular Dystrophy
    9. Stem Cell Therapy
    10. Neuromuscular and Muscle Diseases
    11. Author index
    12. Table of Contents
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      Mechanisms regulating skeletal muscle growth and atrophy (pages 4294–4314)

      Stefano Schiaffino, Kenneth A. Dyar, Stefano Ciciliot, Bert Blaauw and Marco Sandri

      Article first published online: 17 APR 2013 | DOI: 10.1111/febs.12253

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      Muscle growth and atrophy reflect the balance between protein synthesis and protein degradation. Positive and negative regulators of muscle growth, such as the IGF1-Akt and the myostatin-Smad2/3 pathway, respectively, modulate the activity of mTOR and protein synthesis. Protein degradation via the proteasomal and autophagic-lysosomal systems is controlled by FoxO and NF-κB transcription factors.

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      Understanding ALS: new therapeutic approaches (pages 4315–4322)

      Antonio Musarò

      Article first published online: 3 JAN 2013 | DOI: 10.1111/febs.12087

      Thumbnail image of graphical abstract

      Amyotrophic lateral sclerosis (ALS) is a multi-factorial and multi-systemic disease in which alterations in structural, physiological and metabolic parameters in motor neurons, glia, and muscle act synergistically to propagate and exacerbate the disease.

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      Mechanisms of impaired differentiation in rhabdomyosarcoma (pages 4323–4334)

      Charles Keller and Denis C. Guttridge

      Article first published online: 31 JUL 2013 | DOI: 10.1111/febs.12421

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      Rhabdomyosarcomas (RMS) are the most common soft tissue sarcoma of childhood cancers, which are diagnosed by their associated lineage to skeletal muscle. Although these tumors express terminally differentiation markers, they nevertheless aggressively proliferate and are unable to properly differentiate. In this review, we provide a current overview of the various pathways proposed that when dysregulated contribute to the impaired differentiation of both eRMS and aRMS subtypes.

  10. Author index

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Introduction
    5. Mechanisms of Myogenesis
    6. Satellite Cells and Muscle Stem Cells
    7. Muscle Fibrosis and Inflammation
    8. Muscular Dystrophy
    9. Stem Cell Therapy
    10. Neuromuscular and Muscle Diseases
    11. Author index
    12. Table of Contents
    1. You have free access to this content
      Author index (page 4335)

      Article first published online: 20 AUG 2013 | DOI: 10.1111/j.1742-4658.2013.08791.x

  11. Table of Contents

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Introduction
    5. Mechanisms of Myogenesis
    6. Satellite Cells and Muscle Stem Cells
    7. Muscle Fibrosis and Inflammation
    8. Muscular Dystrophy
    9. Stem Cell Therapy
    10. Neuromuscular and Muscle Diseases
    11. Author index
    12. Table of Contents
    1. You have free access to this content
      Table of Contents (page 4336)

      Article first published online: 20 AUG 2013 | DOI: 10.1111/febs.12476

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