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A new strategy for the treatment of diabetic nephropathy : regulation of AMPK/ACC pathway in podocyte.

Research Project

Project/Area Number 21591130
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Metabolomics
Research InstitutionShiga University of Medical Science

Principal Investigator

ISSHIKI Keiji  滋賀医科大学, 医学部, 助教 (60378487)

Co-Investigator(Kenkyū-buntansha) MAEDA Shiro  独立行政法人理化学研究所, 内分泌代謝疾患研究チーム, チームリーダー (50314159)
Project Period (FY) 2009 – 2011
Project Status Completed (Fiscal Year 2011)
Budget Amount *help
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
KeywordsAcetyl-CoA carboxylase beta(ACCβ) / 5' AMP-activated protein kinase(AMPK) / 糸球体上皮細胞 / 糖尿病性腎症 / 腎内脂肪毒性 / Acetyl-CoA carboxylase beta (ACCβ) / 5' AMP-activated protein kinase (AMPK) / 糖尿病 / 脂質 / 脂質代謝異常
Research Abstract

Podocyte-specific overexpression of ACCbeta, a lipogenic enzyme, causes apoptosis, inflammation and reduction of slit-diaphragm proteins in podocytes. These structural and functional abnormalities in podocytes are related to the increase of albuminuria. The activation of AMPK, which suppresses the activity of ACCbeta, may be a new therapeutic target of podocyte injury in diabetic nephropathy by inhibiting the activity of ACCbeta in podocytes

Report

(4 results)
  • 2011 Annual Research Report   Final Research Report ( PDF )
  • 2010 Annual Research Report
  • 2009 Annual Research Report

URL: 

Published: 2009-04-01   Modified: 2016-04-21  

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