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Medical Video: Stem Cell Therapy for Duchenne Muscular Dystrophy: Caleb Sizemore
A healthy person has an average muscle mass of about 54 percent, but people with muscular dystrophy (MD) can have no muscle at all in the final stages of this disease.
What is muscular dystrophy?
Muscular dystrophy or muscular dystrophy is a group of diseases that cause progressive muscle weakness and loss of muscle mass. In muscular dystrophy, gene mutations interfere with the production of proteins needed to form healthy muscles.
This mutation gene is often inherited from parents, but it does not rule out the possibility that mutation genes will develop independently without inheritance.
There are various types of muscular dystrophy - depending on which muscles are affected and what symptoms are caused. The symptom of the most common type of muscular dystrophy, Duchenne MD, starts in childhood, which is easy to fall when moving quickly on a flat road. Muscular dystrophy is more common in boys, while women are only carriers of nature. Other types of dystrophy will not appear until someone has grown up.
Some people with muscular dystrophy will eventually lose the ability to walk. Others may have breathing or swallowing problems.
Muscle-forming proteins can be a solution to muscular dystrophy
There is no antidote for muscular dystrophy, but various therapies can help with physical disabilities and other problems that might develop, including:
- Mobility assistance, such as light exercise, physiotherapy, and physical aids
- Support group, to deal with practical and emotional impacts
- Surgery, to correct posture defects, such as scoliosis
- Drug, such as steroids to increase muscle strength, or ACE inhibitors and beta-blockers to treat heart problems.
New research is looking for ways to improve genetic mutations and damaged muscles associated with MD symptoms. One of them is two separate studies from Rockefeller University and Edinburgh University.
Muscles consist of millions of dense cells. Even in adults, these muscles will continue to regenerate to repair damage that may be caused by various things, illness or injury.
Reporting from Science Dailywhile some new muscles are formed from proteins in stem cells that are responsible for muscle structure and function, mutations arise from fragments of pericyte and PICs, a group of stem cells that can produce fat or muscle.
So far, researchers only know that proteins are indeed involved in muscle formation, but they still don't know how these proteins affect the genes responsible for developing healthy muscles.
"Cell formation whether being muscle or fat, based on our research, is based on a complex protein called laminin," said Yao Yao, assistant professor at the University of Minnesota.
Developing new drugs by acting on the laminin pathway can alleviate many of the symptoms of muscular dystrophy, Yao said further.
Yao's research revealed that the loss of laminin in the body could at least cause some forms of muscular dystrophy. More specifically, Yao and his team focused research on laminin in pericytes and PICs.
Yao and the team conducted a study on a group of mice that showed laminin deficiency in the body. They found that this group of mice had a smaller body shape than other normal mice and had muscle mass below normal. In fact, pericytes and PICs only have a small portion of muscle stem cells, which should not show such dramatic results.
Yao and the team reasoned that replacing laminin in this tissue could help rats recover. However, this idea is considered quite difficult to realize for humans. Although the group of mice showed significant changes - tissue addition and muscle strength - however, injection of laminin in humans would require hundreds of injections so that laminin could be absorbed into the tissue properly.
The scientists then focused their attention on understanding how laminin affects pericytes and PICs to form muscles. They found that laminin affects which genes are activated and not.
One of the 'unique' genes is gpihbp1, which is generally found in capillary pericytes. The gpihbp1 gene has been shown to contribute to fat formation. When laminin is absent, gpihbp1 will no longer be activated in pericytes and PICs.
Based on a number of these ideas, scientists suspect that gpihbp1 might be able to push stem cells to change to form muscles rather than fat. They get around that pericytes and laminin defects to activate gpihbp1, and find that these cells then develop into new muscles.
The research team is now looking for drugs that can increase levels of gpihbp1 in pericytes and PICs, with the aim of providing a way out for many of the symptoms of this disabling disease.
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