Development of a method to suppress the severity of chronic kidney disease through elucidation of mechanism of transition from acute kidney injury

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K08614
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 53040:Nephrology-related
• Research Institution: Saitama Medical University
• Principal Investigator: Okada Hirokazu 埼玉医科大学, 医学部, 教授 (60233342)
• Co-Investigator(Kenkyū-buntansha): 井上 勉 埼玉医科大学, 医学部, 教授 (30406475)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 慢性腎臓病 / 急性腎障害 / 腎線維化

Outline of Final Research Achievements

In AKI due to ischemia or urinary tract obstruction, renal tubular epithelial cells are damaged, resulting in the appearance of cell cycle arrested cells, which may acquire profibrotic traits and cause the onset and progression of renal fibrosis. These G2/M-phase resting cells were induced by renal tubular injury, and the number and survival period increased according to the degree of injury.　Suppression of this cell-targeted profibrotic trait is expected to be developed into an anti-CKD therapy.

Free Research Field

腎臓病学

Academic Significance and Societal Importance of the Research Achievements

慢性腎臓病（CKD)の原因となる病変は腎線維化であり、その発症・進展メカニズムの一つは急性腎障害（AKI)の反復とされている。我々はAKIモデルマウスの腎尿細管上皮細胞の一部に細胞周期停止細胞が出現し、線維化促進性の形質を獲得している可能性を示唆するデータを得た。この細胞の線維化促進性の形質を抑制する治療を開発することで、AKI後のCKDの発症・進展に対する治療に結び付けることが期待できる。