Progression of podocyte disease

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K09685
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Kidney internal medicine
• Research Institution: University of Tsukuba
• Principal Investigator: Nagata Michio 筑波大学, 医学医療系, 教授 (10192238)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: ポドサイト / 糸球体硬化 / 糸球体ろ過

Outline of Final Research Achievements

We performed two sets of experiments using podocyte selective toxin model.
1.Electron microscopically mapping of podocyte injury/detachment showed glomerular pathophysiology, including filtrate and anatomical characteristics of glomerular position and structures is prerequisite for podocyte detachment and segmental sclerosis. 2.Injured podocyte expressed cell migration-driving chemokines, MIF and SDF1, which stimulate migration of parietal cells by expressing their common receptor, CXCR4 chemokines. After podocyte detachment, autocrine mechanism of chemokines and their receptor in PEC promote segmental sclerosis after podocyte loss.

Free Research Field

腎臓病理学

Academic Significance and Societal Importance of the Research Achievements

ポドサイト研究は慢性腎臓病CKDの共通のメカニズムとして広く知られており、本研究はポドサイト障害と糸球体クオカとの因果関係についてびょうりがくてきに、その特性と背景分枝かを明らかにしたものである。このポドサイト特異的障害モデルを用いた2つの研究は、大変ユニークであり、CKDの機序を理解することに貢献したと考えている。