Metabolic Reprogramming and Hypoxic Memory in Kidney Disease

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04835
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Kidney internal medicine
• Research Institution: The University of Tokyo
• Principal Investigator: Nangaku Masaomi 東京大学, 医学部附属病院, 教授 (90311620)
• Co-Investigator(Kenkyū-buntansha): 川上 貴久 東京大学, 医学部附属病院, 助教 (10722093) ; 稲城 玲子 東京大学, 医学部附属病院, 特任准教授 (50232509) ; 田中 哲洋 東京大学, 医学部附属病院, 講師 (90508079) ; 加藤 秀樹 東京大学, 医学部附属病院, 講師 (90625237) ; 正路 久美 東京大学, 医学部附属病院, 病院診療医 (00439423) ; 三村 維真理 東京大学, 医学部附属病院, 助教 (00727084) ; 和田 健彦 東海大学, 医学部, 准教授 (90447409)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 低酸素 / ＨＩＦ / 慢性腎臓病 / 腎不全 / エネルギー代謝 / エピジェネティクス

Outline of Final Research Achievements

Cultured tubular cells and endothelial cells exposed to hypoxia demonstrated changes in expression levels of genes related to energy metabolism and fibrosis. Fibrogenic responses by tubular cells cultured under hypoxic conditions are likely to be regulated by synergistic effects of transcriptional factors.
We developed a novel phosphorescence probe that allows accurate measurement of oxygen tensions of the kidney in vivo. We observed decreases in oxygen tensions in the kidney of animals with anemia or diabetes, and we also found hypoxia of the kidney after acute kidney injury leading to fibrosis. Furthermore, we improved this hypoxia-induced fibrosis after acute kidney injury by performing epigenetic interventions.

Free Research Field

腎臓内科学