Atsushi Higashitani , D.Sc. | Tohoku; Takeshi Nikawa, Ph.D., M.D. | Tokushima University; Takeshi Kobayashi, D.Sc. | Nagoya University; Mika Teranishi , Ph.D. | Tohoku University
Competition Sponsor: Japan Agency for Medical Research and Development
Awardee Year: 2020
Age-related frailty and decreased physical activity cause progressive loss of muscle mass and function, also known as sarcopenia or disuse atrophy. However, the molecular mechanisms underlying sarcopenia and disuse atrophy are poorly understood. Therefore, therapeutic approaches are limited. Recently, we found that intracellular organelle, mitochondria, can sense mechanical stress and generate a signaling factor maintaining muscular homeostasis. Actually, we have confirmed that genetic disruption of mitochondrial mechano-sensing or -signal transduction system contributes to abnormality in homoeostasis of skeletal muscle. On the basis of our findings, we are now exploring pharmacological, nutritional or physical interventions to activate mitochondrial functions. At the same time, using animal models, we will verify the validity of those in stabilizing, alleviating and reversing sarcopenia or disuse atrophy. It not only improves the quality of life for individuals, but also significantly reduces the burden on caregivers and the social costs of public health.
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View this project poster, first displayed at the 2021 Global Innovator Summit.