2009 Fiscal Year Final Research Report
Mechanism of podocyte injury
| Project/Area Number |
18209030
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tokai University |
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Principal Investigator |
MATSUSAKA Taiji Tokai University, 医学部, 准教授 (50317749)
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| Co-Investigator(Kenkyū-buntansha) |
ICHIKAWA Iekuni 東海大学, 医学部, 教授 (80317768)
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| Project Period (FY) |
2006 – 2009
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| Keywords | 糸球体硬化症 / ポドサイト / 蛋白尿 / キメラマウス / SV40 / HIV-1 / トランスジェニックマウス / 慢性腎不全 |
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| Research Abstract |
When the kidney does not function due to diabetes or nephritis, patients need to have lifelong dialysis or renal replacement therapy. Also, they have increased risk for heart and vascular diseases. In this situation, a specialized type of kidney cells, named podocytes, are lost. We tried to increase the number of podocytes which do not normally proliferate after birth, but podocyte proliferation caused kidney injury. We also found that injury in a fraction of podocytes causes injury in other initially intact podocytes, thus forming a vicious cycle toward total loss of podocytes.
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[Journal Article] The CXCL12 (SDF-1)/CXCR4 axis is essential for the development of renal vasculature.2009
Author(s)
Takabatake Y, Sugiyama T, Kohara H, Matsusaka T, Kurihara H, Koni PA, Nagasawa Y, Hamano T, Matsui I, Kawada N, Imai E, Nagasawa T, Rakugi H, Isaka Y.
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Journal Title
J Am Soc Nephrol. 20
Pages: 1714-23
Peer Reviewed
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