To identify the mechanisms that maintain cardiac plasticity in response to hemodynamic stress by elucidating the process of muscle maturation in the syncytium.
Yuki Katanosaka
College of Pharmacy, Kinjo Gakuin University
Selected publications
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Katanosaka Y*, Iwasaki K, Ujihara Y, Takatsu S, Nishitsuji K, Kanagawa M, Sudo A, Toda T, Katanosaka K, Mohri S, Naruse K. TRPV2 is critical for cardiac function and compensatory hypertrophic response to hemodynamic stress. Nature Communications, 2014, DOI:10.1038/ncomms4932.
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Ujihara Y, Kanagawa M, Mohri S, Takatsu S, Kobayashi K, Naruse K, Katanosaka Y*. Elimination of fukutin reveals cellular and molecular pathomechanisms in muscular dystrophy-associated heart failure. Nature Communications, 2019, Doi:10.1038/s41467-019-13623-2.
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Nakamoto H, Katanosaka Y, Chijimatsu R, Mori D, Xaun F et. al., Involvement of TRPV2 in the induction of Lublin and suppression of ectopic endochondral ossification in mouse articular cartilage. Arthiritis Rheumatol. 2021, 73; 1441-1450. Doi: 10.1002/art.41684.
Group A04 (Katanosaka)
Maintenance of cardiac plasticity through critical membrane site control by resilience mediator TRPV2