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“The development of effective therapeutics to target fibrosis is greatly needed to increase both the quality and quantity of life for current DMD patients,” David Hammers said. “This need will continue, even when advancements in gene therapy or gene editing are capable of turning DMD into a milder form of disease, of which fibrosis will still be a feature.”
David Hammers, research assistant professor at the College of Medicine, University of Florida in Gainesville, was awarded an MDA development grant totaling $180,000 over three years to improve understanding of fibrosis in Duchenne muscular dystrophy (DMD)-affected muscle.
In DMD, skeletal muscle degenerates and is replaced with non-functional connective tissue in a process called fibrosis.
To better understand fibrosis in DMD, Hammers and colleagues are investigating the role of cells in the muscle stroma (connective tissue cells) that appear to be in an inappropriate state of senescence, or growth arrest. In other diseases, senescent cells can secrete repair-inhibiting factors and drive fibrosis.
Using a DMD mouse model, Hammers is working to characterize the senescent cells, including determining their numbers, their ability to grow and whether they secrete factors that affect fibrosis. Additionally, he plans to assess whether an enzyme called NOX4 plays a role in causing cellular senescence, and whether it could be targeted with a drug to treat muscle fibrosis in DMD.
If successful, Hammers’ work could provide detailed information about a novel mechanism of muscle fibrosis and help pinpoint new therapeutic targets for the development of anti-fibrotic therapeutics in DMD.
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