gu / ULR7-723-628-227-129-918-314-016-99-72-66-52-41-28-1ort0l71-5261-1201-1201-2101-11noC300200100Figure 3. ROS levels of MCM-iPSC-CMs. H2O2 was measured using ROS-Glo H2O2 assay.おわりに謝 辞引用文献 1. Tokuyama T et al: Disease modeling of mitochondrial cardiomyopathy using patient-specific induced ― 299 ―In this study, I demonstrated that MCM-iPSC-CMs with various genetic mutations partly recapitulated the disease phenotypes, such as cell hypertrophy, abnormal sarcomere structure, mitochondrial dysfunction, and disrupted Ca2+ handling. These MCM-iPSC-CMs disease models provide a much-needed platform for future research on disease pathophysiology and potential drug development. However, further improvement to better recapitulate disease phenotype is still required. I gratefully acknowledge guidance, technical support, and helpful discussions from all members in the Division of Regenerative Medicine, Jichi Medical University, including Prof. Yutaka Hanazono, Prof. Hideki Uosaki, and Takeshi Tokuyama, Nawin Chanthra, Fuad Gandhi-Torizal, Tatsuya Anzai, Kumiko A Iwabuchi, Tomoyuki Abe, Hiromasa Hara, and Rie Ishihara.pluripotent stem cells. Biology, 10 (10), 981 (2021). doi:10.3390/biology101009812. Jimenez-Tellez et al: Cellular models for human cardiomyopathy: What is the best option?. World Journal of Cardiology, 11 (10), 221 (2019). doi:10.4330/wjc.v11.i10.2213. Ahmed RE et al: Sarcomere shortening of pluripotent stem cell-derived cardiomyocytes using fluorescent-tagged sarcomere proteins. JoVE, 3 (169), 62129 (2021). doi:10.3791/62129
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