If physical education does not help
Scientists have identified a compound that stimulates muscle cells in mice
Anna Yudina, "Scientific Russia"
Researchers at the University of California at Los Angeles have identified a compound that can reproduce the effect of exercise on muscle cells in mice, according to a press release from Scientists identify compound that stimulates muscle cells in mice. The results are published in the journal Cell Reports Medicine (Liu et al., A Small-Molecule Approach to Restore a Slow-Oxidative Phenotype and Defective CaMKIIß Signaling in Limb Girdle Muscular Dystrophy) – VM.
Usually muscles become stronger as they are used due to a series of chemical signals inside muscle cells. A newly identified compound activates these signals, suggesting that similar compounds may eventually be used to treat people with limb girdle muscular dystrophy, a form of muscular dystrophy that develops during adolescence.
When muscles don't work regularly, they gradually atrophy. (This phenomenon is familiar to everyone who has been wearing a cast on his leg for several weeks). Fortunately, for people with healthy muscles, this deterioration is reversible. The use of muscles stimulates chemical mediators inside muscle cells that increase muscle mass and strength.
People with limb girdle muscular dystrophy have a genetic defect that interferes with this chemical mediator, making their muscles unable to respond to exercise. No amount of exercise can trigger a signal to strengthen their muscles. Since the muscles are never aware of physical exertion, they gradually wither, and people with this disease find themselves in wheelchairs, almost completely paralyzed.
"It's really dramatic. When these patients lose muscle, they struggle to regain it," said Melissa Spencer, senior author of the paper and a member of the Eli and Edith Center for Regenerative Medicine and Stem Cell Research at UCLA.
The genetic defect responsible for muscular dystrophy of the limb girdle causes a deficiency of an enzyme in muscle cells called CaMK. CaMK is responsible for triggering a chain of chemical signals that turn on genes to increase the cell's ability to grow and metabolize fat, which is used as an energy source.
"CaMK activates genes that promote muscle growth and fat metabolism," said Spencer, who is also a professor of neurology and director of the neuromuscular program at the David Geffen School of Medicine at UCLA.
To find a drug that could help restore the signals associated with CaMK, Spencer and her colleagues, along with Robert Damoiseau, director of the Molecular Shared Screening Resource at the University of California, Los Angeles, tested more than 2,000 compounds to see which ones work in laboratory muscle cells. So far, they have tested 14 promising candidates on mice that had a genetic defect comparable to the defect that causes muscular dystrophy of the limb girdle in humans.
Testing revealed a chemical compound called AMBMP, which allows the muscles of mice to work and grow in the same way as healthy muscle cells.
"When we injected the drug into mice, we found that it activates CaMK and restores all the properties that we observed as defective in our disease model," Spencer said.
Spencer and her collaborators are planning further research to understand how AMBMP affects CaMK and identify similar compounds that may be more effective for humans.
John Vargehese, professor of neurology at the University of California at Los Angeles, associate Professor Irina Kramerova and researcher Jesus Campagna, co-authors of the new study, are already producing new compounds similar to AMBMP. Spencer and Kramerova will test these compounds in mice to determine the best candidate for a drug for clinical trials.
If one of these compounds is effective in human muscles, it will be an important step for the treatment of people with muscular dystrophy of the limb girdle, as well as people whose muscles have atrophied for other reasons – because they have been bedridden for a long time due to illness or injury, for example.
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