This Article  • Full text  • PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Topic Collections  • Cardiovascular Disease/ Myocardial Infarction  • Alert me on articles by topic  Social Bookmarking   What's this?

Tracy Hampton, PhD

JAMA. 2007;298:1152.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

An overabundance of natural antioxidants can lead to heart failure in mice carrying a mutation linked to a human condition known as desmin-related myopathy, report researchers led by scientists at the University of Utah, in Salt Lake City (Rajasekaran NS et al. Cell. 2007;130[3]:427-439). In this disorder, an accumulation of certain proteins leads to myopathy, including cardiomyopathy.

Mice with the mutation develop the same symptoms seen in human patients, including heart enlargement, progressive heart failure, and early death. Although the investigators anticipated seeing high levels of oxidative stress in the animals, they found that the animals' hearts were under reductive stress due to an abundance of a natural antioxidant known as glutathione.

The hearts of the mutant mice exhibited heightened stress responses that yielded reactive oxygen species, triggering antioxidative pathways in which oxidized glutathione was recycled to its reduced, antioxidant form. Overactivity of this pathway produced . . . [Full Text of this Article]

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?