Their findings will inform efforts to identify therapeutics that could inhibit muscle atrophy caused by a chronic reduction in muscle use. Such treatments could end the muscle loss, weakness, and fatigue that can plague space travelers, sedentary or bed-ridden individuals, or anyone whose muscles undergo long periods of disuse.
"By understanding the genes necessary for muscle atrophy," says Kandarian, lead researcher and professor of health sciences at BU Sargent College of Health and Rehabilitation Sciences, "we can begin to study the protein products required for atrophy. Our ongoing research shows that the process of atrophy might be partially moderated by something as straightforward as aspirin or other non-steroidal anti-inflammatory drugs [NSAIDs]."
It is well known that prolonged muscle disuse causes muscles to lose protein in two ways: by decreasing the amount of protein synthesized and by increasing the rate at which muscle protein is degraded. The intracellular signals that drive muscle protein to these extremes, however, are not well known.
When designing her study, Kandarian chose to investigate the role of nfb1 and bcl3, two gene members from a family of transcription factors -- genes that produce proteins that regulate the activities of other genes. Her previous research had shown these transcriptional regulators were implicated in the process of muscle atrophy.