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Investigation of new heart failure onset mechanism by mitochondrial aging-related protein GLO1

Research Project

Project/Area Number 25860580
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Cardiovascular medicine
Research InstitutionYamagata University

Principal Investigator

FUNAYAMA Akira  山形大学, 医学部, 医員 (70642495)

Project Period (FY) 2013-04-01 – 2015-03-31
Project Status Completed (Fiscal Year 2014)
Budget Amount *help
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords心不全 / Glyoxilase 1
Outline of Final Research Achievements

At the onset of heart failure, the decrease in myocardial cell function relates to cardiomyocyte aging. However, the detailed molecular mechanism underlying cardiomyocyte aging is still not well understood. GLO1is present in cell mitochondria, and has been reported to exhibit an anti-aging effect. The aim of this study is to explain the role of GLO1 within the cardiomyocyte. Using cultured cardiomyocyte, we performed a quantitative analysis of GLO1 levels under stimulation. The GLO1 showed a tendency to decrease owing to the stimulation, compared to the pre-stimulation, but no significant decrease was observed.To study whether methyl glyoxilase (MG), which is a GLO1 downstream substance, is related to the prognosis for heart failure patients, the MG blood concentration of those patients was measured. It was found that the high MG group showed a significant relationship with a high number of cardiac deaths. However, no significant correlation was observed between the disease severity.

Report

(3 results)
  • 2014 Annual Research Report   Final Research Report ( PDF )
  • 2013 Research-status Report

URL: 

Published: 2014-07-25   Modified: 2019-07-29  

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