fe in treating hypertension in all age groups and more importantly, known to block TGF-beta activity. Losartan treatment over six months "completely restored muscle architecture" and vastly improved strength, according to Dietz.
Further study pinpointed how too much TGF-beta activity leads to this weakened muscle architecture. According to Ronald Cohn, M.D., lead author on this study, normal muscle, by mobilizing muscle stem cells, can repair itself after injury. The team discovered that excessive TGF-beta blocks muscle regeneration and repair. "The simplest things can injure muscle," explains Cohn, an assistant professor of pediatrics and neurology at Hopkins. "Running a mile down the street causes microscopic tears in leg muscles, which normally go unnoticed because muscles are so efficient at repairing themselves."
Dietz's team then wondered whether the muscle improvement from blocking TGF-beta was specific to Marfan syndrome or possibly represented a strategy that could be applied to other muscle diseases such as Duchenne muscular dystrophy (DMD). Duchenne muscular dystrophy, the most common form of incurable muscular dystrophy in children, generally leads to death in early adulthood or before. DMD causes muscle fibers to be incredibly fragile. As a person with DMD ages, their muscles slowly lose the ability to regenerate and repair, which leads to loss of muscle function, explains Cohn.
TGF-beta never had been implicated as a cause of the inability to repair muscle in DMD. So the researchers examined muscles from mice genetically engineered to have DMD and found evidence of increased TGF-beta activity.
The team treated one group of DMD mice with TGF-beta-blocking protein and another group with losartan. Both groups of treated mice showed completely restored ability to regenerate muscle after injury, whereas untreated mice had large patches of scar tissue in place of muscle. Losartan treatment over many months preservedPage: 1 2 3 Related medicine news :1
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