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Bridget M. Kuehn

JAMA. 2007;298:1385-1386.

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

Although 20 years have elapsed since scientists identified the protein encoded by the defective gene that causes Duchenne muscular dystrophy (DMD), treatment options to help slow the disease's progressive muscle degeneration have remained limited.

In recent years, however, therapeutic prospects have become brighter. Scientists focusing on the disease have developed some promising potential treatments, some of which are in clinical trials. In addition, a few researchers from outside the field have made some fortuitous discoveries about muscle maintenance and regeneration that are providing insights that may one day lead to new treatments.

Muscle from healthy mice has normal architecture (top left), while mdx mice (a model for Duchenne muscular dystrophy) show muscle degradation (top right) that is thought to be related, in part, to excessive activity of transforming growth factor (TGF-). Giving anti–TGF- or the hypertension drug losartan helps restore muscle of mdx mice to more . . . [Full Text of this Article]

BOOSTING GENE EXPRESSION