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2014 Fiscal Year Final Research Report

Mechanisms of progression of chronic kidney disease

Research Project

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Project/Area Number 22249033
Research Category

Grant-in-Aid for Scientific Research (A)

Allocation TypeSingle-year Grants
Section一般
Research Field Kidney internal medicine
Research InstitutionTokai University

Principal Investigator

MATSUSAKA Taiji  東海大学, 医学部, 准教授 (50317749)

Co-Investigator(Kenkyū-buntansha) ICHIKAWA Iekuni  東海大学, 医学部, 客員教授 (80317768)
NIIMURA Fumio  東海大学, 医学部・小児科学, 准教授 (30282750)
NISHIYAMA Akira  香川大学, 医学部・薬理学, 教授 (10325334)
Research Collaborator CAMPBELL Duncan J.  St. Vincent's Institute of Medical Research, Australia, Professor
PASTAN Ira  National Institutes of Health, Bethesda, Maryland, Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Professor
柳田 素子  京都大学医学部, 大学院医学研究科, 教授
Project Period (FY) 2010-04-01 – 2015-03-31
KeywordsAngiotensinⅡ / Angiotensinogen / ポドサイト / 慢性腎不全 / ノックアウトマウス / Magalin / 糸球体硬化症 / ネフローゼ症候群
Outline of Final Research Achievements

In chronic kidney diseases caused by diabetes or nephritis, the key event is injury in a unique type of cells, called podocytes. Podocyte injury triggers progressive deterioration of kidney function. In the present study, we established a method to comprehensively analyze gene expression selectively in podocytes. We also revealed the mechanism underlining induction of angiotensin II within the kidney. Angiotensin II is the most potent blood pressure-raising hormone, and also may further worsen kidney injury. Podocyte injury causes leakage of angiotensinogen, the precursor protein of angiotensin II, which is reabsorbed by kidney cells, and then converted to angiotensin II. This finding provides an insight into mechanism underlining progressive worsening of kidney diseases.

Free Research Field

腎臓病

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Published: 2016-06-03  

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