Table of contents:
A healthy person has an average muscle mass of about 54 percent, but a person with muscular dystrophy (MD) may have no muscle at all in the late stages of the 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 build healthy muscle.
These mutated genes are often inherited from parents, but it is possible that the mutated genes will develop independently without inherited traits.
There are different types of muscular dystrophy - depending on which muscles are affected and what symptoms are causing them. The symptom of the most common type of muscular dystrophy, Duchenne MD, starts in childhood, which is easy falls while moving quickly on uneven roads. Muscular dystrophy is more common in boys, while girls are only carriers. Other types of dystrophy do not appear until a person is an adult.
Some people with muscular dystrophy eventually lose the ability to walk. Others may have trouble breathing or swallowing.
Muscle building proteins can be a solution for muscular dystrophy
There is no antidote for muscular dystrophy, but various therapies can help with physical disabilities and other problems that may develop, including:
- Mobility assistance, such as light exercise, physiotherapy, and physical aids
- Support group, to deal with practical and emotional impacts
- Surgery, to correct postural 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 correct the genetic mutations and damaged muscle associated with MD symptoms. One of these are two separate studies from Rockefeller University and Edinburgh University.
Muscles are made up of millions of solid cells. Even in adults, these muscles will continue to regenerate to repair damage that may be caused by various things, disease or injury.
Reporting from Science Daily, while some new muscle is 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, the researchers only knew that protein was involved in building muscle, but they still didn't know how the protein affected the genes responsible for developing healthy muscle.
"The formation of cells whether into muscle or fat, according to our research, is based on a complex protein called laminin," said Yao Yao, an assistant professor at the University of Minnesota.
Developing new drugs that act on the laminin pathway could relieve many of the symptoms of muscular dystrophy, said Yao further.
Yao's research reveals that the loss of laminin in the body can at least cause some form of muscular dystrophy. More specifically, Yao and his team focused their research on laminin in pericytes and PICs.
Yao and his team conducted a study on a group of mice that showed a deficiency of laminin in the body. They found that this group of mice were smaller than normal mice and had sub-normal muscle mass. In fact, pericytes and PICs only have a small portion of muscle stem cells, which shouldn't show such dramatic results.
Yao and the team reasoned that replacing the laminin in this tissue could help the mice recover. However, this idea is quite difficult to realize for humans. Although this group of mice showed significant changes - increased tissue and muscle strength - however, injection of laminin in humans would require hundreds of injections for the laminin to be absorbed into the tissue properly.
The scientists then focused their attention on understanding how laminin affects the pericytes and PICs to build muscle. They found that laminin affects which genes are activated and which are not.
One of these "unique" genes is "gpihbp1“, Which are generally found in the capillaries where pericytes live. Gen "gpihbp1"Has been shown to have a role in the formation of fat. When laminin isn't present, "gpihbp1Will no longer be enabled on pericytes and PICs.
Starting from these ideas, scientists suspect that gpihbp1 might be able to encourage stem cells to change to form muscle rather than fat. They got around to laminin deficient pericytes and PICs to activate gpihbp1, and found that these cells then developed into new muscle.
The research team is now looking for drugs that can increase the levels of gpihbp1 in pericytes and PICs, with the aim of providing a solution for many of the symptoms of this debilitating disease.
