肌肉细胞 z-bo 2020-10-26 369

　　Researchers at the University of California, Los Angeles have identified a compound that can replicate the effects of exercise in the muscle cells of mice.

　　Generally, muscles become stronger when used due to a series of chemical signals inside muscle cells. The newly discovered compound activates these signals, suggesting that similar compounds can eventually be used to treat people with psoas muscle dystrophy, a form of adolescent muscular dystrophy.

　　When muscles cannot work properly, they gradually atrophy. (This phenomenon is familiar to people who have been casting spells on the legs for several weeks.) Fortunately, for people with healthy muscles, this deterioration is reversible. Muscle use stimulates chemical messengers inside muscle cells, thereby increasing muscle mass and strength.

　　People with muscular dystrophy have a genetic defect in limb girdle muscular dystrophy, which interferes with the chemical messenger and prevents their muscles from responding to exercise. No exercise can trigger signals to strengthen muscles. Because muscles can never get information, they gradually wither, and people with this disease end up almost completely paralyzed in a wheelchair.

　　The senior author of the paper, Melissa Spencer, a member of the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at the University of California, Los Angeles (UCLA), said: “It’s really compelling. It’s difficult for them to regain muscles when they are muscles.

　　The genetic defect that causes belt-like muscular dystrophy in the extremities causes muscle cells called CaMK to lack an enzyme. CaMK is responsible for emitting a series of chemical signals that turn on genes to enhance the ability of cells to grow and metabolize fat, and fat is used as energy.

　　Spencer said: "CaMK activates genes that promote muscle growth and fat metabolism," he is also a professor of neurology and director of the neuromuscular program at the David Geffen School of Medicine at UCLA.

　　In order to find a drug that can help restore signals related to CaMK, Spencer and her colleagues screened more than 2,000 compounds with Robert Damoiseaux, UCLA Molecular Shared Screening Resource Director, to see which compounds act in muscle cells grown in the laboratory. effect. So far, they have tested 14 promising candidates in mice with genetic defects comparable to mice that cause human limb girdle muscular dystrophy.

　　The

　　 test identified a compound called AMBMP, which can make the muscles of mice work and grow in the form of healthy muscle cells.

　　Spencer said: "When we put this drug into mice, we found that it activated CaMK and restored all the defects we observed in disease models."

　　Spencer and her collaborators are planning further studies to understand how AMBMP affects CaMK and identify similar compounds that are more effective in the human body.