A study on ER-stress-induced Fanconi syndrome

2020 Fiscal Year Final Research Report

• Project/Area Number: 18H02348
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Review Section: Basic Section 42020:Veterinary medical science-related
• Research Institution: University of Miyazaki
• Principal Investigator: IKEDA Masahiro 宮崎大学, 農学部, 教授 (60281218)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: 薬理学 / 小胞体ストレス / Fanconi症候群 / 腎虚血再灌流障害

Outline of Final Research Achievements

Although Fanconi syndrome is a multifactorial disease, its clinical features are based on reduced reabsorption of water, solutes, and nutrients in the kidneys, especially in the proximal tubules. So far, the mechanism by which the common symptom of reabsorption deficiency occurs largely unknown. From this study, we have identified a new mechanism of renal endoplasmic reticulum stress for this deficiency. Also, we have shown that at least two gene expressions are directly linked to the symptom. These results provide important information for human and veterinary clinical fields and indicate a new regulatory system for substance metabolism in the kidney.

Free Research Field

獣医薬理学

Academic Significance and Societal Importance of the Research Achievements

Fanconi症候群は、先天性のものから、化学物質誘導型および疾患続発型と多岐の要因で生じる疾患である。しかしながら多くの場合、腎におけるアミノ酸などの再吸収不全という共通の症状を示す。本研究では、この共通の症状を示すメカニズムとして腎の小胞体ストレスを同定している。この成果は、Fanconi症候群の今後の診断・治療法の開発に貢献することに加えて、物質の腎における再吸収や分泌の新しい視座を与え、生理学的にも重要な意味を持つ。