Establishment of the molecualr basis underlying regulation of cardiac redox homeostasis by electrophilic signaling and its therapeutic application for heart failure
| Project/Area Number |
25670031
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Biological pharmacy
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| Research Institution | Okazaki Research Facilities, National Institutes of Natural Sciences |
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Principal Investigator |
NISHIDA Motohiro 大学共同利用機関法人自然科学研究機構(岡崎共通研究施設), 岡崎統合バイオサイエンスセンター, 教授 (90342641)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 活性酸素 / 硫黄 / 循環 / 心不全 / 活性イオウ / レドックス / 心臓 / 親電子 / 生物系薬学 / 心血管 / Ｇタンパク質 / 翻訳後修飾 |
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| Outline of Final Research Achievements |
We have reported the possibility that hydrogen sulfide anion (H2S/HS-) protects against chronic heart failure via nucleophilic elimination of endogenous electrophiles in mouse hearts after myocardial infarction. However, it is still obscure whether H2S/HS- acts as a molecular entity of reactive nucleophile in hearts. In this study, we aim to identify the molecular entity of nucleophilic reactive sulfur species (RSS) in hearts and establish an innovative strategy based on the to treat chronic heart failure. We found that proteins containing cysteine persulfide or polysulfide acts as RSS, and accumulation of RSS by taking a polysulfur (garlic)-containing diet dramatically suppresses cardiac risk after myocardial infarction in mice. These results strongly suggest that preservation of RSS in heart will be a novel strategy to reduce cardiac risk.
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Report
(3 results)
Research Products
(20 results)
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[Journal Article] Inhibition of N-type Ca2+ channels ameliorates an imbalance in cardiac autonomic nerve activity and prevents lethal arrhythmias in mice with heart failure.2014
Author(s)
Yamada Y, Kinoshita H, Kuwahara K, Nakagawa Y, Kuwabara Y, Minami T, Yamada C, Shibata J, Nakao K, Cho K, Arai Y, Yasuno S, Nishikimi T, Ueshima K, Kamakura S, Nishida M, Kiyonaka S, Mori Y, Kimura T, Kangawa K, Nakao K.
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Journal Title
Cardiovasc Res.
Volume: 104
Pages: 183-193
NAID
Related Report
Peer Reviewed
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[Journal Article] GRK6 deficiency in mice causes autoimmune disease due to impaired apoptotic cell clearance2013
Author(s)
Nakaya M, Tajima M, Kosako H, Nakaya T, Hashimoto A, Watari K, Nishihara H, Ohba M, Komiya S, Tani N, Nishida M, Taniguchi H, Sato Y, Matsumoto M, Tsuda M, Kuroda M, Inoue K, Kurose H
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Journal Title
Nature Commun
Volume: 4
Issue: 1
Pages: 1532-1532
DOI
Related Report
Peer Reviewed
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[Journal Article] Atrial natriuretic peptide-mediated inhibition of microcirculatory endothelial Ca2+ and permeability response to histamine involves cGMP-dependent protein kinase I and TRPC6 channels.2013
Author(s)
Chen W, Oberwinkler H, Werner F, Gaßner B, Nakagawa H, Feil R, Hofmann F, Schlossmann J, Dietrich A, Gudermann T, Nishida M, Del Galdo S, Wieland T, Kuhn M.
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Journal Title
Arterioscler Thromb Vasc Biol.
Volume: 33
Issue: 9
Pages: 2121-2129
DOI
Related Report
Peer Reviewed
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