Kang Jong-soons research team at the College of Medicine presents the possibility of developing a cure for aging muscular dystrophy

Since skeletal muscle, which accounts for about 40% of the bodys body, consumes and stores the largest amount of energy in the bodys organs, and secrete various myokines during activity, the deterioration and reduction of skeletal muscle can have a very serious effect on the body. Osteoporosis caused by aging, chronic disease, and decreased physical activity exacerbates the prevalence and symptoms of secondary diseases such as metabolic disease, chronic inflammation, cardiovascular disease and cancer, thereby increasing mortality.

The pace of aging in our country is unprecedentedly radical. According to data from Statistics Korea in 2019, Koreas ratio of people aged 65 or older is 37 percent in 2045, surpassing that of Japan, the worlds No. 1 aging society. Aging musculoskeletal muscle depletion (Sarcopenia) was classified as a disease in the U.S. and Europe from 2016-2018, and various global pharmaceutical companies have tried to develop treatments as an urgent part of the treatment development, but there are no treatments to date. Aging myocardium has a variety of basal mechanisms, such as mitochondria active changes in muscles, protein metabolic changes, and loss of regenerative powers such as early aging of stem cells.

In the lab of Kang Jong-soon, a professor at SKKU medical school, we are working to develop a cure for senile myopia while carrying out various molecular electromagnet studies in relation to muscle aging. Two recent studies on muscle aging were published in Journal of Cachexia, Sarcopenia and Muscle (imfact factor 10.75), the top journal of the field, back to back on February 27. The studies were conducted jointly with the Mount Sinai School of Medicine and the DGIST research team in New York, the United States.

The second paper found that Indopropen, a drug that Kim Hye-bin, a student of this lab, can participate as the first author to perform mitochondria active control in muscles, has the effect of controlling muscle function reduction and muscle consumption in aging mice. This effect has been found not only to increase energy efficiency through the activation of mitochnodria in aging muscle, but also to suppress protein breakdown while promoting protein synthesis. This was established by activating AKT/S6K pathways, a protein synthesis device, through direct coupling to PDK1. The report of excessive protein decomposition and decreased protein synthesis in neurosis of aging is expected to be a clue to the development of a treatment that is critical to controlling aging or disease-related myopia.