2016 Fiscal Year Final Research Report
Involvement of acidification of glomerular cells by AGE-cholesterol-aggregated proteins in development of diabetic nephropathy
| Project/Area Number |
26460635
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Applied pharmacology
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| Research Institution | Meijo University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
TAKAHASHI Kazuo 藤田保健衛生大学, 医学部, 講師 (90631391)
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| Research Collaborator |
YAMADA Shigeki
HAYASHI Takahiro
HIRASAWA Yasushi
FENG Yibin
AKIYAMA Shinichi
YUZAWA Yukio
UCHIYA Keiichi
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 糖尿病性腎症 / 糖化凝集タンパク質 / コレステロール |
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| Outline of Final Research Achievements |
We have demonstrated the validity of our hypothesis regarding the development of diabetic nephropathy, which was as follows: AGE-cholesterol-aggregated albumin (ACAA) is formed in the blood flow of diabetic patients, and taken up in glomerular mesangial cells to achieve the breakdown of ACAA in lysosome. Simultaneously, mitochondria of mesangial cells are activated, and mesangial cells are acidified followed by an increase in pro-inflammatory cytokine expression. The cytokines induce inflammation in the glomeruli repeatedly, resulting in diabetic nephropathy. We also clarified the mechanisms for protecting mesangial cells from acidification due to ACAA or an acidic environment. Additionally, our results suggested that ACAA causes damage in mesangial mitochondria followed by apoptosis.
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| Free Research Field |
腎薬理学
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