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Sci. Signal., 7 August 2012
Vol. 5, Issue 236, p. pc18
[DOI: 10.1126/scisignal.2003426]


Science Signaling Podcast: 7 August 2012

Christopher W. Ward1, Ramzi J. Khairallah2, Eric P. Hoffman3, and Annalisa M. VanHook4

1 University of Maryland School of Nursing, Baltimore, MD 21201, USA.
2 Center for Biomedical Engineering and Technology (BioMET) and the Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
3 Research Center for Genetic Medicine, Children's National Medical Center, and Department of Integrative Systems Biology, George Washington University, Washington, DC 20010, USA.
4 Web Editor, Science Signaling, American Association for the Advancement of Science, 1200 New York Avenue, NW, Washington, DC 20005, USA.

Abstract: This Podcast features an interview with Christopher Ward, Ramzi Khairallah, and Eric Hoffman, authors of a Research Article published in the 7 August 2012 issue of Science Signaling. Duchenne muscular dystrophy (DMD) is an inherited, degenerative muscle disease that is caused by mutations in the gene that encodes dystrophin, which is part of the cytoskeleton in muscle cells. DMD is a progressive disease that causes muscle weakness, leading to paralysis and eventually death. In a mouse model of DMD and in human patients, there is increased calcium influx into muscle cells and increased production of reactive oxygen species in muscle cells, but how these phenomena are connected to the cytoskeleton and to muscle degeneration are not well understood. In their new study, Ward, Khairallah, Hoffmann, and colleagues have explored the mechanism by which reactive oxygen species affects DMD muscle cells. Their results suggest that reducing microtubule density or preventing the production of reactive oxygen species in skeletal muscle might slow the progression of Duchenne muscular dystrophy.

Citation: C. W. Ward, R. J. Khairallah, E. P. Hoffman, A. M. VanHook, Science Signaling Podcast: 7 August 2012. Sci. Signal. 5, pc18 (2012).

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