Brief Communications

Loss of myostatin attenuates severity of muscular dystrophy in mdx mice

  1. Kathryn R. Wagner MD, PhD1,
  2. Alexandra C. McPherron PhD2,
  3. Nicole Winik BS2,
  4. Se-Jin Lee MD, PhD2,*

Article first published online: 4 NOV 2002

DOI: 10.1002/ana.10385

Issue

Annals of Neurology

Annals of Neurology

Volume 52, Issue 6, pages 832–836, December 2002

Additional Information

How to Cite

Wagner, K. R., McPherron, A. C., Winik, N. and Lee, S.-J. (2002), Loss of myostatin attenuates severity of muscular dystrophy in mdx mice. Annals of Neurology, 52: 832–836. doi: 10.1002/ana.10385

Author Information

  1. 1

    Departments of Neurology and

  2. 2

    Molecular Biology and Genetics, The Johns Hopkins University, School of Medicine, Baltimore, MD

*Department of Molecular Biology and Genetics, The Johns Hopkins School of Medicine, 725 N. Wolfe Street, Baltimore, MD 21205

Publication History

  1. Issue published online: 22 NOV 2002
  2. Article first published online: 4 NOV 2002
  3. Manuscript Revised: 6 AUG 2002
  4. Manuscript Accepted: 6 AUG 2002
  5. Manuscript Received: 7 JUN 2002

Funded by

  • NIH. Grant Numbers: R01HD35887, 1K08NS02212
  • Duchenne Parent Project
  • Muscular Dystrophy Association

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Abstract

Myostatin, a transforming growth factor–β family member, is a negative regulator of skeletal muscle growth. To explore the therapeutic potential of targeting myostatin in settings of muscle degeneration, we crossed myostatin null mutant mice with mdx mice, a model for Duchenne and Becker muscular dystrophy. Mdx mice lacking myostatin were stronger and more muscular than their mdx counterparts. Diaphragm muscle showed less fibrosis and fatty remodeling, suggesting improved muscle regeneration.

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