Mitsuharu OKUTSU
- Division
- Biological Science, Associate Professor
- Academic Degree
- Ph.D.
| Research Field | Molecular Biology and Cellular Physiology of Exercise |
|---|---|
| Keywords | skeletal muscle, atherosclerosis, exercise |
| Current Research Topics | (1) How to prevent against cachectic factor-induced skeletal muscle atrophy: Cachectic factor induces skeletal muscle atrophy. Exercise training prevents against skeletal muscle atrophy, however, little is known about the underlying mechanisms. A goal in our lab is to establish the factor “X” to prevent against skeletal muscle atrophy. (2) Molecular mechanism of prevention against atherosclerosis by exercise: Exercise training prevents the development of atherosclerosis. Our goal in this project is to identify and determine the molecular mechanism in exercise-induced protection of endothelial cell damage (dysfunction) in atherosclerosis. |
| Selected Publications | (Orignal Articles) Regular exercise stimulates endothelium autophagy via IL-1 signaling in ApoE deficient mice. FASEB J, 35:e21698 (2021). Muscle-derived SDF-1α/CXCL12 modulates endothelial cell proliferation but not exercise training-induced angiogenesis. Am J Physiol Regul Integr Comp Physiol, 317:R770-R779.(2019). p62/SQSTM1 and Nrf2 are essential for exercise-mediated enhancement of antioxidant protein expression in oxidative muscle. FASEB J, 33:8022-8032 (2019). Muscle-derived extracellular superoxide dismutase inhibits endothelial activation and protects against multiple organ dysfunction syndrome in mice. Free Radic Biol Med, 113:212-223 (2017). ADAM12: a genetic modifier of preclinical peripheral arterial disease. Am J Physiol Heart Circ Physiol, 309:H790-803 (2015). Enhanced skeletal muscle expression of extracellular superoxide dismutase mitigates streptozotocin-induced diabetic cardiomyopathy by reducing oxidative stress and aberrant cell signaling. Circulation: Heart Failure, 8:188-97 (2015). Extracellular superoxide dismutase ameliorates skeletal muscle abnormalities, cachexia and exercise intolerance in mice with congestive heart failure. Circulation: Heart Failure, 7:519-30 (2014). Exercise prevents maternal high-fat diet-induced hypermethylation of the Pgc-1α gene and age-dependent metabolic dysfunction in the offspring. Diabetes, 63:1605-11 (2014). Corticosterone accelerates atherosclerosis in the apolipoprotein E-deficient mouse. Atherosclerosis, 232:414-9 (2014). Disconnecting mitochondrial content from respiratory chain capacity in PGC-1-deficient skeletal muscle. Cell Rep, 3:1449-56 (2013). Autophagy is required for exercise training-induced skeletal muscle adaptation and improvement of physical performance. FASEB J, 27:4184-93 (2013). Baf60c drives glycolytic metabolism in the muscle and improves systemic glucose homeostasis through Deptor-mediated Akt activation. Nature Medicine, 19:640-5 (2013). A novel PGC-1α isoform induced by resistance training regulates skeletal muscle hypertrophy. Cell, 151:1319-31 (2012). Kruppel-like factor 15 regulates skeletal muscle lipid flux and exercise adaptation. Proc Natl Acad Sci U S A, 109:6739-44 (2012). Translational suppression of atrophic regulators by microRNA-23a integrates resistance to skeletal muscle atrophy. J Biol Chem, 286:38456-65 (2011). Cortisol-induced CXCR4 augmentation mobilizes T lymphocytes after acute physical stress. Am J Physiol Regul Integr Comp Physiol, 288:R591-9 (2005). (Review Articles) 骨格筋の恒常性維持に関する最新知見. 体力科学, 67(3):245-249 (2018). |