Dystrophic heart failure blocked by membrane sealant poloxamer

Soichiro Yasuda, DeWayne Townsend, Daniel E. Michele, Elizabeth G. Favre, Sharlene M. Day and Joseph M. Metzger ()
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Soichiro Yasuda: Departments of Molecular and Integrative Physiology
DeWayne Townsend: Departments of Molecular and Integrative Physiology
Daniel E. Michele: Departments of Molecular and Integrative Physiology
Elizabeth G. Favre: Departments of Molecular and Integrative Physiology
Sharlene M. Day: University of Michigan
Joseph M. Metzger: Departments of Molecular and Integrative Physiology

Nature, 2005, vol. 436, issue 7053, 1025-1029

Abstract: Muscular dystrophy Heart failure accounts for at least 15% of deaths in Duchenne muscular dystrophy, and as palliative treatments for the skeletal muscle aspects of the disease improve, this proportion is rising. Experiments on cardiac myocytes from normal and dystrophin-deficient (mdx) mice, and in whole animals, show that the primary defect in the dystrophic heart is heightened susceptibility to intracellular calcium overload. This can be corrected by repairing the damaged membrane with a sealant, Poloxamer 188 (P188), and mdx animals pre-treated with P188 are protected from cardiac failure. This work suggests that sealants that act like P188 might be developed as therapeutics for muscular dystrophy and other diseases of membrane instability.

Date: 2005
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DOI: 10.1038/nature03844

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