They are Tokyo Medical and Dental University.
Maintaining a regular workout regimen can help you look and feel great, but it can also help maintain your muscles and bones. People who are unable to engage in physical activity weaken their muscles and bones. Researchers in Japan have found a new drug that may aid in the treatment of locomotor frailties by inducing similar effects as exercise.
sarcopenia and osteoporosis can be caused by physical inactiveness. Increasing muscle strength and bone formation can be achieved by exercising. Exercise therapy can’t be applied to all cases. Drug therapy can be helpful in treating sarcopenia and osteoporosis when patients have dementia or cerebrovascular disease. There is not a single drug that addresses both issues at the same time.
A novel drug screening system was developed by researchers from the Tokyo Medical and Dental University to identify a compound that mimics the changes in muscle and bone that occur as a result of exercise. The researchers used the screening system to identify the aminoindazole derivatives. The growth of muscle cells and bone-forming cells could be stimulated by LAMZ.
There were no obvious side effects when LAMZ was administrated to mice. According to Takehito Ono, lead author of the study, LAMZ-treated mice exhibited larger muscle fiber width, greater maximal muscle strength, and a higher rate of bone formation.
The mode of function of LAMZ was further addressed by the research team and they found it to be similar to calcium and PGC-1 signaling pathways. The pathways that are activated during exercise are involved in maintaining muscle and bone.
An animal model that has sarcopenia and osteoporosis was administrated to the team to see if LAMZ could treat locomotor frailties. Senior author Tomoki Nakashima says the drug improved the muscles and bones of the mice.
The research team’s findings show that LAMZ represents a potential therapeutic method for the treatment of locomotor frailties.
More information: Takehito Ono et al, Simultaneous augmentation of muscle and bone by locomomimetism through calcium-PGC-1α signaling, Bone Research (2022). DOI: 10.1038/s41413-022-00225-w Provided by Tokyo Medical and Dental University