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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2020.1
- 수록면
- 124 - 139 (16page)
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Canonical Transient Receptor Potential Channels and Vascular Smooth Muscle Cell Plasticity Motohiro Nishida,1,2,3,4 Tomohiro Tanaka,1,2,3 Supachoke Mangmool,5 Kazuhiro Nishiyama,4 and Akiyuki Nishimura4 1National Institute for Physiological Sciences and Exploratory Research Center on Life and Living Systems, National Institutes of Natural Sciences, Aichi 444-8787, Japan. 2Department of Physiological Sciences, SOKENDAI (School of Life Science, The Graduate University for Advanced Studies), Aichi 444-8787, Japan. 3Center for Novel Science Initiatives (CNSI), NINS, Tokyo 105-0001, Japan. 4Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan. 5Faculty of Science, Mahidol University, Bangkok 10400, Thailand. Correspondence to Motohiro Nishida, Ph.D. Division of Cardiocirculatory Signaling, National Institute for Physiological Sciences and Exploratory Research Center on Life and Living Systems, National Institutes of Natural Sciences, Higashiyama 5-1, Myodaiji-cho, Okazaki, Aichi 444-8787, Japan. Email: nishida@nips.ac.jp Received November 29, 2019; Revised January 02, 2020; Accepted January 03, 2020. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Go to: Abstract Vascular smooth muscle cells (VSMCs) play a pivotal role in the stability and tonic regulation of vascular homeostasis. VSMCs can switch back and forth between highly proliferative (synthetic) and fully differentiated (contractile) phenotypes in response to changes in the vessel environment. Abnormal phenotypic switching of VSMCs is a distinctive characteristic of vascular disorders, including atherosclerosis, pulmonary hypertension, stroke, and peripheral artery disease; however, how the control of VSMC phenotypic switching is dysregulated under pathological conditions remains obscure. Canonical transient receptor potential (TRPC) channels have attracted attention as a key regulator of pathological phenotype switching in VSMCs. Several TRPC subfamily member proteins—especially TRPC1 and TRPC6—are upregulated in pathological VSMCs, and pharmacological inhibition of TRPC channel activity has been reported to improve hypertensive vascular remodeling in rodents. This review summarizes the current understanding of the role of TRPC channels in cardiovascular plasticity, including our recent finding that TRPC6 participates in aberrant VSMC phenotype switching under ischemic conditions, and discusses the therapeutic potential of TRPC channels.
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참고문헌 (106)
참고문헌 신청
Owens GK / 2004 / Molecular regulation of vascular smooth muscle cell differentiation in development and disease / Physiol Rev 84:767~801
Rensen SS / 2007 / Regulation and characteristics of vascular smooth muscle cell phenotypic diversity / Neth Heart J 15:100~108
Owens GK / 1982 / Alterations in vascular smooth muscle mass in the spontaneously hypertensive rat. Role of cellular hypertrophy, hyperploidy, and hyperplasia / Circ Res 51:280~289
Owens GK / 1983 / Vascular smooth muscle cell hypertrophy and hyperploidy in the Goldblatt hypertensive rat / Circ Res 53:491~501
Owens GK / 1989 / Control of hypertrophic versus hyperplastic growth of vascular smooth muscle cells / Am J Physiol 257:H1755~H1765
Rensen SS / 2007 / Regulation and characteristics of vascular smooth muscle cell phenotypic diversity / Neth Heart J 15:100~108
Owens GK / 1982 / Alterations in vascular smooth muscle mass in the spontaneously hypertensive rat. Role of cellular hypertrophy, hyperploidy, and hyperplasia / Circ Res 51:280~289
Owens GK / 1983 / Vascular smooth muscle cell hypertrophy and hyperploidy in the Goldblatt hypertensive rat / Circ Res 53:491~501
Owens GK / 1989 / Control of hypertrophic versus hyperplastic growth of vascular smooth muscle cells / Am J Physiol 257:H1755~H1765
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