2012 Fiscal Year Final Research Report
The roleof H_20_2as an endothelium-derived relaxing factors (EDRFs)
| Project Area | Signaling functions of reactive oxygen species |
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| Project/Area Number |
20117009
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| Research Category |
Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SATOH Kimio 東北大学, 高等教育開発推進センター, 准教授 (80436120)
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| Project Period (FY) |
2008 – 2012
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| Keywords | 血管内皮 / 内皮由来弛緩因子 / 一酸化窒素 / 過酸化水素 / 一酸化窒素合成酵素 |
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| Research Abstract |
Oxidative stress, generated by excessive reactive oxygen species (ROS) promotes cardiovascular disease. However, the precise mechanism how ROS (i.e., H_20_2,0_2', and 'OH)deteriorate vascular function and promote vascular remodeling has not been clearly elucidated. Moreover, H_20_2 also plays a crucial role as a signaling molecule under physiological conditions. Our recent study revealed that H_20_2 is one of the endothelium-derived hyperpolarizing factor (EDHF) that contributes as a signaling molecule in the Vasculature.
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