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Elucidation of molecular mechanisms and development of vascular complications in diabetic nephropathy and renal arteriosclerosis

Research Project

Project/Area Number 15K09265
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Kidney internal medicine
Research InstitutionThe University of Tokushima

Principal Investigator

ABE Hideharu  徳島大学, 大学院医歯薬学研究部(医学系), 准教授 (60399342)

Co-Investigator(Kenkyū-buntansha) 村上 太一  徳島大学, 大学院医歯薬学研究部(医学系), 助教 (30403736)
Project Period (FY) 2015-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Keywords糖尿病性腎症 / 腎硬化症 / 腎臓病修復学 / Smad1 / BMP4 / 糸球体硬化 / 糖尿病 / 加齢 / 細胞老化 / 細動脈硬化
Outline of Final Research Achievements

In diabetic kidney disease (DKD), incipient diabetic nephropathy is classically defined by increasing albuminuria, heralding a decline in glomerular filtration rate (GFR). However, a proportion of patients with type 2 diabetes does not follow this classical albuminuric pathway. Varying degrees of arteriosclerosis were seen in the subjects with normoalbuminuria. We previously found that Smad1 plays a critical role in the development of DKD both in vitro and in vivo. However, functional interaction between Smad1 and Smad3 signaling in DKD is unclear. Extracellular matrix (ECM) protein overexpression and Smad1 activation were observed in the glomeruli of db/db mice but were suppressed in the glomeruli of Smad3-KO-DKD mice. Smad3 activation enhanced the phosphorylation of Smad1 C-terminal domain but decreased the phosphorylation of linker domain. Collectively, preferential activation of the Smad1 linker domain may provide a novel therapeutic approach for treating DKD.

Report

(4 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report
  • 2015 Research-status Report
  • Research Products

    (7 results)

All 2018 2017 2016 2015

All Journal Article (4 results) (of which Int'l Joint Research: 3 results,  Peer Reviewed: 4 results,  Open Access: 3 results,  Acknowledgement Compliant: 1 results) Presentation (2 results) (of which Int'l Joint Research: 1 results) Patent(Industrial Property Rights) (1 results) (of which Overseas: 1 results)

  • [Journal Article] Urinary IgG4 and Smad1 are Specific Biomarkers for Renal Structural and Functional Changes in Early Stage of Diabetic Nephropathy.2018

    • Author(s)
      Doi T, Moriya T, Fujita Y, Minagawa N, Usami M, Sasaki T, Abe H, Kishi S, Murakami T, Ouchi M, Ichien G, Yamamoto K, Ikeda H, Koezuka Y, Takamatsu N, Shima K, Mauer M, Nagai K, Tominaga T.
    • Journal Title

      Diabetes

      Volume: 67 Issue: 5 Pages: 986-993

    • DOI

      10.2337/db17-1043

    • Related Report
      2017 Annual Research Report
    • Peer Reviewed / Open Access / Int'l Joint Research
  • [Journal Article] Probucol modulates Nrf2 function and ameliorates diabetic nephropathy in db/db mice.2017

    • Author(s)
      Arai H, Abe H, Sakurai A, Yamashita K, Murayama T, Minami M, Yoshikawa T, Kohashi M, Nozako M, Yokode M, Doi T.
    • Journal Title

      Medical Research Archives.

      Volume: 4 Pages: 1-16

    • Related Report
      2016 Research-status Report
    • Peer Reviewed / Open Access / Acknowledgement Compliant
  • [Journal Article] Conditional Deletion of Smad1 Ameliorates Glomerular Injury in Progressive Glomerulonephritis2016

    • Author(s)
      Araki M, Matsubara T, Abe H, Torikoshi K, Mima A, Iehara N, Fukatsu A, Kita T, Arai H, Doi T
    • Journal Title

      Sci Rep

      Volume: 6 Issue: 1 Pages: 31216-31216

    • DOI

      10.1038/srep31216

    • NAID

      120006345067

    • Related Report
      2016 Research-status Report
    • Peer Reviewed / Open Access / Int'l Joint Research
  • [Journal Article] Bone Morphogenetic Protein 4 and Smad1 Mediate Extracellular Matrix Production in the Development of Diabetic Nephropathy.2015

    • Author(s)
      Matsubara T, Araki M, Abe H, Ueda O, Jishage K, Mima A, Goto C, Tominaga T, Kinosaki M, Kishi S, Nagai K, Iehara N, Fukushima N, Kita T, Arai H, Doi T.
    • Journal Title

      Diabetes

      Volume: 64 Issue: 8 Pages: 2978-2990

    • DOI

      10.2337/db14-0893

    • Related Report
      2015 Research-status Report
    • Peer Reviewed / Int'l Joint Research
  • [Presentation] 糖尿病性腎症の糸球体硬化抑制過程におけるSmad1の新規リン酸化部位の同定と解析2017

    • Author(s)
      小野広幸、安部秀斉, 上田紗代、西村賢二、田蒔昌憲、村上太一, 岸誠司, 長井幸二郎, 土井俊夫
    • Organizer
      第255回徳島医学会学術集会
    • Related Report
      2017 Annual Research Report
  • [Presentation] The Role of BMP4 Signal Pathway on the Podocyte Injury in Diabetic Early Stage.2016

    • Author(s)
      Fujita Y, Tominaga T, Murakami T, Kishi S, Nagai K, Abe H, Doi T
    • Organizer
      49th American Society of Nephrology (ASN) Annual Meeting
    • Place of Presentation
      Chicago, IL, U.S.A
    • Year and Date
      2016-11-15
    • Related Report
      2016 Research-status Report
    • Int'l Joint Research
  • [Patent(Industrial Property Rights)] 腎臓様組織の製造方法2017

    • Inventor(s)
      安部秀斉
    • Industrial Property Rights Holder
      国立大学法人徳島大学
    • Industrial Property Rights Type
      特許
    • Filing Date
      2017
    • Related Report
      2017 Annual Research Report
    • Overseas

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Published: 2015-04-16   Modified: 2019-03-29  

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