The development of a novel therapeutic strategies for chronic kidney disease by the targeting on the renal mitochondrial oxidative stress.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25293193
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Kidney internal medicine
• Research Institution: Tohoku University
• Principal Investigator: MORI TAKEFUMI 東北大学, 医学(系)研究科(研究院), 准教授 (40375001)
• Co-Investigator(Kenkyū-buntansha): ITO SADAYOSHI 東北大学, 大学院医学系研究科, 教授 (40271613) ; KIYOMOTO HIDEYASU 東北大学, メディカルメガバンク機構, 教授 (00304585) ; OHSAKI YUSUKE 東北大学, 大学院医学系研究科, 助教 (40509212)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 腎臓 / 酸化ストレス / ミトコンドリア / 蛍光イメージング / アンジオテンシンII / グルコース / 低酸素

Outline of Final Research Achievements

The effects on the reactive oxygen species production of physiological stimuli were assessed in renal medullary thick ascending limb of loop of Henle (mTAL) in rats. Angiotensin II stimulation increased the intracellular ROS concentration through mitochondrial ROS production in mTAL. High concentration of glucose stimulated the mitochondrial ROS production via the glucose degradation products. Hypoxia also increased mitochondrial ROS production. The administration of mitoTEMPO, which is scavenger of mitochondrial ROS, attenuated the reduction of renal medullary blood flow and oxygen concentration induced by ischemia/reperfusion.

Free Research Field

腎臓生理学