Discovery of resistance genes against tubular interstitial disorders.

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K06474
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 42040:Laboratory animal science-related
• Research Institution: Kitasato University
• Principal Investigator: SASAKI NOBUYA 北里大学, 獣医学部, 教授 (20302614)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 腎臓病 / 尿細管間質障害 / マウスモデル / 慢性腎臓病 / 連鎖解析

Outline of Final Research Achievements

In advanced countries, as the number of chronic kidney disease (CKD) patients increases, the enormous medical expenses associated with their prognosis have become a problem, and the development of treatments has become urgent. The onset of CKD involves many lifestyle risk factors such as diabetes, hypertension, hypercholesterolemia, obesity, and smoking, and the number of CKD pre-patients is increasing. The applicant identified a resistance locus to tubulointerstitial injury (renal fibrosis and renal anemia), which is the cause of renal dysfunction, by analyzing a CKD model mouse caused by a Tensin2 gene mutation. In this study, candidate genes were determined by whole-genome analysis and RNA-seq analysis using next-generation sequencers, and the tubulointerstitial injury-aggravating gene was identified by creating a gene-modified mouse.

Free Research Field

腎臓病

Academic Significance and Societal Importance of the Research Achievements

本国において、腎不全は病死の原因第5位であり、その予備軍であるCKDは、成人の8人に1人が罹患している国民病であるが未だ根治療法は開発されていない。透析患者数は約33万人にのぼり、年間1万人ずつ増加している。透析患者1人あたりの年間医療費は約500万円であり腎臓病の医療費は年1.5兆円を超える。蛋白尿は尿細管間質障害を徐々に進行させ、最終的にCKDを経て腎不全に至る。したがって、多様な要因(原疾患)を有するCKDの治療において、尿細管間質障害の進行を止める治療が広く効果的であり、人工透析への移行を防止することができる。本研究は、独自のスクリーニング法によって、新規尿細管間質障害を同定した。