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Clinical Science and Biomedicine(Medical and Health Sciences)

Tanaka ShotaAssistant professor

2013.4 – 2016.3
To investigate whether mitochondrial fusion inhibitor, p13, affected cardiac hypertrophy.
2016.4 – 2020.3
To investigate how β-adrenergic stimulation induce inflammation in cardiac fibroblasts and how the inflammation affect cardiac dysfunction.
2020.4 – today
To investigate whether the regulation of mitochondrial kinetics and mitophagy induce cardiomyocytes proliferation.

Research theme

To elucidate whether the amelioration of mitochondrial quality promotes cardiomyocytes proliferation

Mammal’s cardiomyocytes stop proliferation immediately after birth. One of the cause is that the growth of cardiomyocytes accompany by mitochondrial maturation, which increase oxidative stress to inhibit cell cycle. Mitochondria repeat fission and fusion to maintain the quality and hypoactive mitochondria are removed by mitophagy, which is mitochondrial selective autophagy. Accordingly, I aim to elucidate whether the amelioration of mitochondrial quality promotes cardiomyocytes proliferation.

Representative achievements

β2-adrenergic stimulation induces interleukin-6 by increasing Arid5a, a stabilizer of mRNA, through cAMP/PKA/CREB pathway in cardiac fibroblasts.
Shota Tanaka, Atsuki Imaeda, Kotaro Matsumoto, Makiko Maeda, Masanori Obana, Yasushi Fujio
Pharmacology research & perspectives 8(2) e00590 2020 April

Myofibroblast β2 adrenergic signaling amplifies cardiac hypertrophy in mice.
Atsuki Imaeda, Shota Tanaka, Kota Tonegawa, Shota Fuchigami, Masanori Obana, Makiko Maeda, Miho Kihara, Hiroshi Kiyonari, Simon J Conway, Yasushi Fujio, Hiroyuki Nakayama
Biochemical and biophysical research communications 510(1) 149-155 2019 February 26

Caveolae-Specific CaMKII Signaling in the Regulation of Voltage-Dependent Calcium Channel and Cardiac Hypertrophy.
Shota Tanaka, Yasushi Fujio, Hiroyuki Nakayama
Frontiers in physiology 9 1081-1081 2018 August 7