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Keitaro Yamanouchi is a Professor in the Laboratory of Veterinary Physiology, Department of Veterinary Medical Sciences, Graduate School of Agricultural and Life Sciences at The University of Tokyo. He holds a PhD from The University of Tokyo, awarded in October 1996. His academic career at the institution includes positions in the Graduate School of Agricultural and Life Sciences beginning in 1995, with an appointment as Professor in April 2022. He previously served as a Research Fellow in the Muscle Biology Group at the University of Arizona from 2000 to 2001 and conducted research at the University of Pittsburgh from 1992 to 1994.
Yamanouchi’s research focuses on tissue-specific stem and progenitor cells, with particular emphasis on skeletal muscle development, regeneration, differentiation, ageing, and related conditions such as muscular dystrophy. He has developed and utilized animal models, including rat models of Duchenne muscular dystrophy, to investigate mechanisms of muscle regeneration, fat accumulation in muscle, and potential therapeutic approaches. His work also extends to comparative biology perspectives in mammalian life sciences, including applications relevant to veterinary medicine and animal production such as intramuscular fat deposition. In addition to research, he contributes to veterinary medical education through lectures and practical training in physiology, emphasizing active learning. Yamanouchi has received awards including the Japan Veterinary Medical Association Award in 2017 for research on mammalian skeletal muscle development and regeneration, and the first Ito Memorial Foundation Award in 2015. He holds numerous committee and editorial roles, such as serving as editor-in-chief of the journal of the Japanese Society of Veterinary Science since 2023 and as a council member of the Japanese Society for Muscle Research since 2017. He maintains an active publication record with contributions to studies on muscle biology and related fields.
University of Tokyo researchers uncover how p16INK4a in aging muscle fibers exacerbates Duchenne muscular dystrophy, hindering regeneration. p16 knockout and senolytics restore strength—new hope for Japan’s DMD patients.
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