Suzuki, Takeshi



Faculty of Pharmacy, Department of Pharmacy 薬学教育研究センター (Shiba-Kyoritsu)



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Books 【 Display / hide

  • 疾患と薬物治療 第10章 精神疾患.

    鈴木岳之, 藤本和子, 横田恵理子, 井澤早苗., 医歯薬出版, 東京, 2008.05

    Scope: 303-328

  • 通信講座テキスト 第4講座「レセプターと薬の作用機序」.

    鈴木岳之, 藤本和子., 東京/共立薬科大学, 2006.04

    Scope: 1-80

  • 新しい機能形態学−ヒトの成り立ちとその働き.

    小林静子、馬場広子、平井みどり., 東京/広川書店, 2005.06

    Scope: 177-184, 339-347

  • スタンダード薬学シリーズ4 生物系薬学 Ⅰ. 生命体の成り立ち 第5章 循環系.

    鈴木岳之., 東京/東京化学同人, 2005.03

    Scope: 30-33

  • 受容体(レセプター)と薬の作用機序.

    鈴木岳之, 藤本和子., 東京/共立薬科大学, 2004.09

    Scope: 1-

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Papers 【 Display / hide

  • The effect of a synthetic estrogen, ethinylestradiol, on the herg block by e-4031

    Tamura F., Sugimoto S., Sugimoto M., Sakamoto K., Yamaguchi M., Suzuki T., Fukuda K., Ieda M., Kurokawa J.

    Biomolecules (Biomolecules)  11 ( 9 )  2021.09

    Research paper (scientific journal), Joint Work, Accepted

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    Inhibition of K+-conductance through the human ether-a-go-go related gene (hERG) channel leads to QT prolongation and is associated with cardiac arrhythmias. We previously reported that physiological concentrations of some estrogens partially suppress the hERG channel currents by interacting with the S6 residue F656 and increase the sensitivity of hERG blockade by E-4031. Although these studies suggested that clinically used synthetic estrogens with similar structures have the marked potential to alter hERG functions, the hERG interactions with synthetic estrogens have not been assessed. We therefore examined whether ethinylestradiol (EE2), a synthetic estrogen used in oral contraceptives, affects hERG function and blockade by drugs. Supratherapeutic concentrations of EE2 did not alter amplitudes or kinetics of the hERG currents elicited by train pulses at 20 mV (0.1 Hz). On the other hand, EE2 at therapeutic concentrations reduced the degree of hERG current suppression by E-4031. The administration of EE2 followed by E-4031 blockade reversed the current suppression, suggesting that the interaction of EE2 and E-4031 alters hERG at the drug-binding site. The effects of EE2 on hERG blockade raised the possibility that other estrogens, including synthetic estrogens, can alter hERG blockade by drugs that cause QT prolongation and ventricular arrhythmias.

  • Ramelteon modulates gamma oscillations in the rat primary motor cortex during non-REM sleep

    Yoshimoto A., Yamashiro K., Suzuki T., Ikegaya Y., Matsumoto N.

    Journal of Pharmacological Sciences (Journal of Pharmacological Sciences)  145 ( 1 ) 97 - 104 2021.01

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  13478613

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    Sleep disorders adversely affect daily activities and cause physiological and psychiatric problems. The shortcomings of benzodiazepine hypnotics have led to the development of ramelteon, a melatonin MT1 and MT2 agonist. Although the sleep-promoting effects of ramelteon have been documented, few studies have precisely investigated the structure of sleep and neural oscillatory activities. In this study, we recorded electrocorticograms in the primary motor cortex, the primary somatosensory cortex and the olfactory bulb as well as electromyograms in unrestrained rats treated with either ramelteon or vehicle. A neural-oscillation-based algorithm was used to classify the behavior of the rats into three vigilance states (e.g., awake, rapid eye movement (REM) sleep, and non-REM (NREM) sleep). Moreover, we investigated the region-, frequency- and state-specific modulation of extracellular oscillations in the ramelteon-treated rats. We demonstrated that in contrast to benzodiazepine treatment, ramelteon treatment promoted NREM sleep and enhanced fast gamma power in the primary motor cortex during NREM sleep, while REM sleep was unaffected. Gamma oscillations locally coordinate neuronal firing, and thus, ramelteon modulates neural oscillations in sleep states in a unique manner and may contribute to off-line information processing during sleep.

  • Soft Matrix Promotes Cardiac Reprogramming via Inhibition of YAP/TAZ and Suppression of Fibroblast Signatures

    Kurotsu S., Sadahiro T., Fujita R., Tani H., Yamakawa H., Tamura F., Isomi M., Kojima H., Yamada Y., Abe Y., Murakata Y., Akiyama T., Muraoka N., Harada I., Suzuki T., Fukuda K., Ieda M.

    Stem Cell Reports (Stem Cell Reports)  15 ( 3 ) 612 - 628 2020.09

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  22136711

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    © 2020 The Authors In this article, Ieda and colleagues showed that a soft matrix, which is comparable with native myocardium, efficiently promoted cardiac reprogramming. This soft matrix enhanced cardiac reprogramming via inhibition of integrin, Rho/ROCK, actomyosin, and YAP/TAZ signaling and subsequent suppression of fibroblast programs, which were activated on conventional rigid substrates, thus demonstrating that mechanotransduction plays a critical role in cardiac reprogramming.

  • A Comparative Study of the Market Configuration of the Japanese Pharmaceutical Market Using the Gini Coefficient and Herfindahl–Hirschman Index

    Shibata S., Fukumoto D., Suzuki T., Ozaki K.

    Therapeutic Innovation and Regulatory Science (Therapeutic Innovation and Regulatory Science)  54 ( 5 ) 1047 - 1055 2020.09

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  21684790

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    © 2020, The Drug Information Association, Inc. Background: As of 2015, the Japanese pharmaceutical market was the world’s third largest pharmaceutical market. Although previous studies have examined market differences in terms of market size and pricing policy, little is known about comparative market configurations. The present study provides a comparative analysis of pharmaceutical market configurations in Japan and five other markets. Methods: Based on data for the 100 top-selling drugs in 2014 in Japan, the United States, the United Kingdom, France, Germany, and the global market, we explored differences in market configurations using the Herfindahl–Hirschman Index, Lorenz curves, and Gini coefficients. We also investigated market trends by analyzing changes in sales, sales volume, and price. Results: The 100 top-selling drugs accounted for a lower share of the total market in Japan, France, and Germany as compared to the United States and the United Kingdom. The market deviation of the 100 top-selling drugs indicated by the Herfindahl–Hirschman Index and Gini coefficient was smallest in Japan. Sales of most of the top-100 drugs increased in all the countries studied; however, directional price changes differed by country and sales volume trend. Conclusion: Our findings showed that market deviations in Japan were relatively low compared with those in other developed countries, suggesting that some of the more beneficial drugs in other developed countries obtain relatively fewer benefits from the Japanese pharmaceutical market, and some less beneficial drugs obtained more benefits.

  • Perturbation of the titin/MURF1 signaling complex is associated with hypertrophic cardiomyopathy in a fish model and in human patients

    Yuta Higashikuse, Nishant Mittal, Takuro Arimura, Sung Han Yoon, Mayumi Oda, Hirokazu Enomoto, Ruri Kaneda, Fumiyuki Hattori, Takeshi Suzuki, Atsushi Kawakami, Alexander Gasch, Tetsushi Furukawa, Siegfried Labeit, Keiichi Fukuda, Akinori Kimura, Shinji Makino

    Dis Model Mech (DMM Disease Models and Mechanisms)  12 ( 11 )  2019.11

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  17548403

     View Summary

    © 2019. Published by The Company of Biologists Ltd. Hypertrophic cardiomyopathy (HCM) is a hereditary disease characterized by cardiac hypertrophy with diastolic dysfunction. Gene mutations causing HCM have been found in about half of HCM patients, while the genetic etiology and pathogenesis remain unknown for many cases of HCM. To identify novel mechanisms underlying HCM pathogenesis, we generated a cardiovascularmutant medaka fish, non-spring heart (nsh), which showed diastolic dysfunction and hypertrophic myocardium. The nsh homozygotes had fewer myofibrils, disrupted sarcomeres and expressed pathologically stiffer titin isoforms. In addition, the nsh heterozygotes showed M-line disassembly that is similar to the pathological changes found in HCM. Positional cloning revealed a missense mutation in an immunoglobulin (Ig) domain located in the Mline-A-band transition zone of titin. Screening of mutations in 96 unrelated patients with familial HCM, who had no previously implicated mutations in known sarcomeric gene candidates, identified two mutations in Ig domains close to the M-line region of titin. In vitro studies revealed that the mutations found both in medaka fish and in familial HCM increased binding of titin to muscle-specific ring finger protein 1 (MURF1) and enhanced titin degradation by ubiquitination. These findings implicate an impaired interaction between titin and MURF1 as a novel mechanism underlying the pathogenesis of HCM.

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Papers, etc., Registered in KOARA 【 Display / hide

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Reviews, Commentaries, etc. 【 Display / hide

  • Direct reprogramming, epigenetics, and cardiac regeneration.

    Kurotsu S, SUZUKI T, Ieda M

    J Card Fail 23 ( 7 ) 552 - 557 2017

    Article, review, commentary, editorial, etc. (scientific journal), Single Work

Presentations 【 Display / hide

  • 抗うつ薬とP2X4受容体の相互作用の比較検討.

    ○笠原由佳, 三浦麻利衣, 最上由香里, 関野祐子, 佐藤薫, 鈴木岳之.

    日本薬学会第134回年会 (熊本) , 


  • Neural differentiation potentials in human embryonic stem cell lines.

    ○福本大悟, 松本拓也, 岡田洋平, 末盛博文, 中辻憲夫, 鈴木岳之, 赤松和土, 岡野栄之.

    第87回日本薬理学会年会 (仙台) , 


  • 中国医薬品市場の現状と製薬企業の動向分析および今後の展開.

    ○森田和仁, 鈴木岳之.

    第57回日本薬学会関東支部大会 (東京) , 


  • 新薬創出加算の獲得・継続に影響を及ぼす因子の解析.

    ○反町知希, 相川大輔, 中村洋, 鈴木岳之.

    第57回日本薬学会関東支部大会 (東京) , 


  • P2X4 receptor-mediated acceleration of microglial activation is important for the L-glutamate release from activated microglia in the early stage of inflammation.

    Sato K, Fujimori K, Takaki J, Suzuki T, Sekino Y.

    Neuro2013 (京都) , 


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Research Projects of Competitive Funds, etc. 【 Display / hide

  • The pharmaceutical market and drug development prognosis in Japan.


    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Principal investigator


Courses Taught 【 Display / hide











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