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Skeletal muscle

  • REVIEW
    Neuromuscular disease modeling on a chip
    Jeffrey W. Santoso, Megan L. McCain
    Disease Models & Mechanisms 2020 13: dmm044867 doi: 10.1242/dmm.044867 Published 7 July 2020

    Summary: Modeling neuromuscular diseases is challenging due to their complex etiology and pathophysiology. Here, we review the cell sources and tissue-engineering procedures that are being integrated as emerging neuromuscular disease models.

  • RESEARCH ARTICLE
    HCT116 colorectal liver metastases exacerbate muscle wasting in a mouse model for the study of colorectal cancer cachexia
    Joshua R. Huot, Leah J. Novinger, Fabrizio Pin, Andrea Bonetto
    Disease Models & Mechanisms 2020 13: dmm043166 doi: 10.1242/dmm.043166 Published 24 January 2020

    Summary: Colorectal cancer-derived liver metastases exacerbate cachexia, in line with activation of STAT3 signaling. STAT3 inhibition may improve cancer-associated muscle wasting.

  • REVIEW
    Cored in the act: the use of models to understand core myopathies
    Aurora Fusto, Louise A. Moyle, Penney M. Gilbert, Elena Pegoraro
    Disease Models & Mechanisms 2019 12: dmm041368 doi: 10.1242/dmm.041368 Published 19 December 2019

    Summary: The core myopathies are neuromuscular disorders with no cure. In this Review, we outline our current understanding of pathomechanisms, the advantages and limitations of available models, and discuss emerging modeling technologies.

  • RESEARCH ARTICLE
    C9ORF72-related cellular pathology in skeletal myocytes derived from ALS-patient induced pluripotent stem cells
    Eileen Lynch, Theran Semrad, Vincent S. Belsito, Claire FitzGibbons, Megan Reilly, Koji Hayakawa, Masatoshi Suzuki
    Disease Models & Mechanisms 2019 12: dmm039552 doi: 10.1242/dmm.039552 Published 16 August 2019

    Summary: Evidence of protein aggregation and mitochondrial dysfunction were found in skeletal myocytes differentiated from ALS-patient induced pluripotent stem cells with the C9ORF72 mutation.

  • RESEARCH ARTICLE
    Deterioration of mitochondrial bioenergetics and ultrastructure impairment in skeletal muscle of a transgenic minipig model in the early stages of Huntington's disease
    Marie Rodinova, Jana Krizova, Hana Stufkova, Bozena Bohuslavova, Georgina Askeland, Zaneta Dosoudilova, Stefan Juhas, Jana Juhasova, Zdenka Ellederova, Jiri Zeman, Lars Eide, Jan Motlik, Hana Hansikova
    Disease Models & Mechanisms 2019 12: dmm038737 doi: 10.1242/dmm.038737 Published 26 July 2019

    Summary: Specific mitochondrial parameters in muscle of a minipig model of Huntington's disease can be used as potential biomarkers of disease progression and suggest that similar pathogenic mechanisms underlie disease progression in TgHD minipigs and HD patients.

  • REVIEW
    Therapeutic strategies for spinal muscular atrophy: SMN and beyond
    Melissa Bowerman, Catherina G. Becker, Rafael J. Yáñez-Muñoz, Ke Ning, Matthew J. A. Wood, Thomas H. Gillingwater, Kevin Talbot, The UK SMA Research Consortium
    Disease Models & Mechanisms 2017 10: 943-954; doi: 10.1242/dmm.030148

    Summary: Translational research for spinal muscular atrophy (SMA) should address the development of non-CNS and survival motor neuron (SMN)-independent therapeutic approaches to complement and enhance the benefits of CNS-directed and SMN-dependent therapies.

  • RESEARCH ARTICLE
    Poor maternal nutrition and accelerated postnatal growth induces an accelerated aging phenotype and oxidative stress in skeletal muscle of male rats
    Jane L. Tarry-Adkins, Denise S. Fernandez-Twinn, Jian Hua Chen, Iain P. Hargreaves, Viruna Neergheen, Catherine E. Aiken, Susan E. Ozanne
    Disease Models & Mechanisms 2016 9: 1221-1229; doi: 10.1242/dmm.026591

    Summary: Muscle of ‘developmentally programmed’ rat offspring demonstrated accelerated aging and oxidative stress, which could explain why some individuals are at greater risk of developing age-associated muscular dysfunction than others.

  • RESEARCH ARTICLE
    Angiotensin-(1-7) attenuates disuse skeletal muscle atrophy in mice via its receptor, Mas
    María Gabriela Morales, Johanna Abrigo, María José Acuña, Robson A. Santos, Michael Bader, Enrique Brandan, Felipe Simon, Hugo Olguin, Daniel Cabrera, Claudio Cabello-Verrugio
    Disease Models & Mechanisms 2016 9: 441-449; doi: 10.1242/dmm.023390

    Summary: In this article, the authors demonstrate that a peptide with actions mainly in the cardiovascular system prevents the skeletal muscle damage induced by disuse.

  • RESEARCH ARTICLE
    The role of mTOR signaling in the regulation of protein synthesis and muscle mass during immobilization in mice
    Jae-Sung You, Garrett B. Anderson, Matthew S. Dooley, Troy A. Hornberger
    Disease Models & Mechanisms 2015 8: 1059-1069; doi: 10.1242/dmm.019414

    Summary: The activation of mTOR signaling is both necessary and sufficient to alleviate the decreases in protein synthesis and muscle mass that occur during immobilization.

  • RESOURCE ARTICLE
    Phospholamban overexpression in mice causes a centronuclear myopathy-like phenotype
    Val A. Fajardo, Eric Bombardier, Elliott McMillan, Khanh Tran, Brennan J. Wadsworth, Daniel Gamu, Andrew Hopf, Chris Vigna, Ian C. Smith, Catherine Bellissimo, Robin N. Michel, Mark A. Tarnopolsky, Joe Quadrilatero, A. Russell Tupling
    Disease Models & Mechanisms 2015 8: 999-1009; doi: 10.1242/dmm.020859

    Summary: Phospholamban overexpression in mouse slow-twitch muscle impairs SERCA function and causes histopathological features associated with human centronuclear myopathy.

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