2014 Fiscal Year Final Research Report
New concept for treatment of iscgemia/reperfusion injuries brought by metabolomics
| Project/Area Number |
23310136
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Genome biology
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| Research Institution | Keio University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
KUBO Akiko 慶應義塾大学, 医学部, 特任講師 (50455573)
YACHIE Ayako 慶應義塾大学, 医学部, 共同研究員 (10453549)
HISHIKI Takako 慶應義塾大学, 医学部, 講師 (10338022)
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| Project Period (FY) |
2011-04-01 – 2015-03-31
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| Keywords | hypoxia / metabolomics / HIF / PHD / iscemia |
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| Outline of Final Research Achievements |
Cells turn on hypoxic response under the environment where the available oxygen molecules are limited. Hypoxic response is mainly regulated by transcriptional factor HIF (hypoxia-inducible factor), which is also negatively regulated by “oxygen sensor” prolyl-hydroxylase PHDs. Among all PHDs, inactivation of PHD2 alone is sufficient to activate HIF pathway.
Given that hypoxic response is designed for tissue protection under the hypoxic environment such as ischemic diseases, activation of HIF by PHD2-blocade should have beneficial role in ischemia/reperfusion model. Here we reported that inactivation of Phd2 in mice myocardial infarction model revealed smaller infarction size and better cardiac function by maintaining higher ATP with lower oxygen consumption. Our study shed light on new treatment for ischemia reperfusion injuries by targeting oxygen sensor PHD2.
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| Free Research Field |
病態医化学
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