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DMD/BMD — Kass

David Kass (DMD/BMD)
Kass is studying a component of muscle cell membranes called "TRPC" channels which are located in muscle cell membranes. In DMD and in other muscular dystrophies, Kass said, these channels can become "hyperactive" and "leaky," resulting in increased calcium levels inside the cell — a condition that can cause cell damage or death.
Duchenne Muscular Dystrophy (DMD)

MDA has awarded a research grant totaling $210,618 over two years to David Kass, professor of cardiology, medicine and biomedical engineering at Johns Hopkins University in Baltimore. The new funds will help support Kass’ study of the disease process and potential therapeutic strategies in Duchenne (DMD), Becker (BMD) and other muscular dystrophies.

One particular problem in DMD is hyperactive "TRPC" channels in the muscle cell membrane that leak calcium and sodium. These channels can increase calcium levels inside the cell, stimulating oxidative stress, which can lead to cell damage and/or death.

Kass and colleagues recently discovered that a protein called PKG (for protein kinase G) can directly suppress TRPC channels.

Kass plans to test the importance of PKG activation to block stimulated TRPC channels in both heart muscle and skeletal muscle cells in research models of muscular dystrophy, and determine if such modification can inhibit muscle damage associated with excess calcium and oxidative stress.

Findings from Kass’ work may inform development of a treatment based on the pathways relevant to TRPC channel regulation. A number of drugs already approved for treatment of other conditions by the U.S. Food and Drug Administration (including sildenafil, or Viagra) hold potential for this type of treatment.

"It's great to become part of the MDA family, and I am very excited about pursuing the work we are undertaking," Kass said.

Funding for this MDA grant began February 1, 2011.

‹ DMD/BMD — Hoshijima up DMD/BMD — Liu ›

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