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Cardiovascular Research Advance Access originally published online on April 8, 2009
Cardiovascular Research 2009 82(3):383-384; doi:10.1093/cvr/cvp115
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Somatic gene therapy to treat heart failure is one step closer to reality

Muthu Periasamy1,* and Jill A. Rafael-Fortney2

1 Department of Physiology and Cell Biology, College of Medicine and Public Health, The Ohio State University, 304 Hamilton Hall, 1645 Neil Ave, Columbus, Ohio 43210, USA
2 Department of Molecular and Cellular Biochemistry, The Ohio State University, 304 Hamilton Hall, 1645 Neil Ave, Columbus, Ohio 43210, USA

* Corresponding author. Tel: +1 614 292 2310; fax: +1 614 292 4888. E-mail address: periasamy.1@osu.edu

This editorial refers to ‘Prevention of cardiomyopathy in {delta}-sarcoglycan knockout mice after systemic transfer of targeted adeno-associated viral vectors’ by C. Goehringer et al.,6 pp. 404–410, this issue.

The first 10% of the full text of this article appears below.

Despite recent advances in heart failure therapy, patients with end-stage cardiac failure have a poor prognosis and die within 5 years. Diagnosis of the hereditary form of heart failure is becoming increasingly prevalent due to the identification of causative mutations in many structural genes encoding contractile and cytoskeletal proteins. The majority of muscular dystrophies including Duchenne muscular dystrophy (DMD) cause functional deficits not only in skeletal muscle but also in cardiac muscle since the proteins affected are normally present in all striated muscle. DMD is caused by mutations in the very large dystrophin gene. Dystrophin binds the submembranous cytoskeleton at one end and at the other . . . [Full Text of this Article]


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Prevention of cardiomyopathy in {delta}-sarcoglycan knockout mice after systemic transfer of targeted adeno-associated viral vectors
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Cardiovasc Res 2009 82: 404-410. [Abstract] [Full Text] [PDF]