People who can’t exercise often suffer from weak muscles. This may be because of obesity, immobility, frailty, or health complications such as diabetes. Now, there’s hope as Salk scientists are one step closer to finding the treatment for muscle degeneration by using gene editing technology. Together with their collaborators, they found a way to suppress a natural muscle-growth inhibitor on mice and worms, and the result? The subjects acquired super-strength and high-endurance gene edited muscles.
The answer to muscle degeneration
Salk Institute for Biological Studies, together with Swiss institutions, Ecole Polytechnique Federale de Lausanne (EPFL) and the University of Lausanne may have found the treatment for genetics-related or age-related muscle degeneration. How did they do it? They discovered that the strength of our muscles is determined by a tiny inhibitor and modulating the activity of certain genes by acting on a genome regulator (NCoR1) can help make them stronger.
According to Ronald M. Evans, a professor in Salk’s Gene Expression Lab and leader of the Salk team, it may now be possible to help people who are not capable of engaging in physical exercise by developing drugs to address their concern.
The lead author from EPFL, Johan Auwerx, adds that NCoR1 is a type of molecule that acts as brakes which decreases the activity of genes. Once you release the brake by mutation or with chemicals, the gene circuits are reactivated and thus providing more energy to muscle and enhancing its activity. According to him, it could be used to address muscle weakness in the elderly as well as a basis for the development of a treatment for genetic muscular dystrophy.
He also stated that it will surely attract the interest of athletes and medical experts once the results are confirmed in humans.
Denser, more massive Gene edited Muscles
The Salk researchers and their collaborators also reported that by genetically manipulating the offspring of the experimental mice and nematodes, they were able to suppress NCoR1, enabling the muscle tissue to develop more effectively. They also said that the mutated mice didn’t just show higher endurance but better cold tolerance as well. The experiments on nematode worms showed similar results which made them conclude that other living creatures are likely to react the same way. In terms of side effects, they haven’t detected any harmful reactions that are associated with the elimination of the NCoR1 receptor in muscle and fat tissues. The team is also looking into potential drug molecules that could be used to reduce the effectiveness of NCoR1.
What makes the difference? How does suppressing an inhibitor build muscle? Microscopic examination of the mutated muscle fibers shows that they are denser, more massive, and with cells that have higher numbers of mitochondria which are like power generators for metabolic activities.
The researchers are happy with their results which also show great possibilities in long-term therapeutic applications.