动物造模 z-bio 2021-11-29 291

　　Researchers at the University of California, Los Angeles have identified compounds that can replicate exercise effects in mouse muscle cells. The findings were published in the journal Cell Reporting Medicine. Normally, a series of chemical signals in muscle cells make the muscles stronger during use. The newly discovered compound activates these signals, suggesting that similar compounds can eventually be used to treat adolescent muscular dystrophy (a type of muscular dystrophy).

　　 If muscles cannot function properly, they will gradually contract. (This phenomenon is well-known to those who have stepped on their feet for a few weeks.) Fortunately, for people with healthy muscles, this deterioration is reversible. The use of muscle stimulates chemical messengers in muscle cells, thereby increasing muscle mass and strength. People with muscular dystrophy have genetic defects in extremity band muscular dystrophy, which interfere with chemical transmitters and prevent muscles from responding to exercise. Exercise cannot trigger signals to strengthen muscles. As the muscles cannot be touched, they gradually weaken and the patient is almost completely paralyzed in the wheelchair.

　　Melissa Spencer (Melissa Spencer), the lead author of the paper and a member of the Eliand EdytheBroad Center for Regenerative Medicine and Stem Cell Research at the University of California, Los Angeles (UCLA), said: Losing muscles, it is difficult for them to restore muscles. The genetic defect that causes band muscular dystrophy in the extremities requires an enzyme called CaMK in muscle cells. CaMK is responsible for turning on genes and releasing a series of chemical signals, thereby increasing 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 professor of neurology and director of the neuromuscular program at the David Geffen School of Medicine at the University of California, Los Angeles (UCLA). . To find a way to help recover

　　 CaMK-related signaling drugs, Spencer and her colleagues and Robert Damoiseaux, UCLA Molecular Shared Screening Resource Director, screened more than 2,000 compounds in the laboratory. We studied the compounds that grow in muscle cells by kicking. To. So far, they have tested 14 promising candidate genes in mice. The genetic defects of these candidate genes are comparable to those that cause human limb girdle muscular dystrophy. "This test identified a compound called AMBMP. The compound enables mouse muscles to function and grow in the form of healthy muscle cells.

　　 Spencer said: Spencer and her co-authors said: "Putting this drug into mice can activate CaMK and restore all the defects observed in disease models." AMBMP is located in CaMK. We are planning to conduct further research to understand how it affects us. Identify similar compounds that are more effective on the human body.