讲座题目:Maladaptive repair in kidney disease progression
主讲人:Professor Motoko Yanagita
讲座时间:11月23日(周二)16:00 (中国)/ 17:00(日本)
讲座地点:Webex会议
会议连接:
https://kyotomed.webex.com/kyotomed/j.php?MTID=md2f1f8ea2d5558ae4ba98acfd3eca196
嘉宾介绍
Professor Motoko Yanagita
Motoko Yanagita
Professor, Chair, Department of Nephrology, Kyoto University Graduate School of Medicine.
She obtained her doctorate to become M.D.( Medicine) at Kyoto University Faculty of Medicine in 1994, and obtained her doctorate to become Ph.D. (Nephrology) at Kyoto University Graduate School of Medicine in 2001. After postdocoral training at Exploratory Research for Advanced Technology (ERATO), Japan Science and Technology Agency, she became Associate Professor Centers of Excellence (COE) Program of Japan Society for the Promotion of Science, Kyoto University Graduate School of Medicine from 2004 to 2007,Lecturer, Career-Path Promotion Unit, Kyoto University from 2007 to 2010,Associate Professor, Hakubi Project, Young Researcher Promotion Unit, Kyoto University from 2010 to 2011. In 2011,she became Professor, Chair, Department of Nephrology, Kyoto University Graduate School of Medicine. She also hold the post of PI Board member of ASHBi (Institute for the Advanced Study of Human Biology) in 2018.
She was honored as 1st Ishibashi Yukiko Memorial Prize(2018)2nd Prize, Baelz Prize (2020), Kidney International Reviewer of the Year(2020).
Professor Motoko Yanagita’s main Research Topic is identification of cell populations responsible for kidney repair and regeneration and the elucidation of their regulatory mechanisms. She previously identified Gas6 and USAG-1, factors exacerbating kidney disease. In recent years, she demonstrated that renal anemia and fibrosis are caused by the dysfunction of kidney resident fibroblasts, and proximal tubule injury induces the dysfunction of fibroblast causing fibrosis. She further showed that proximal tubule injury also causes distal tubule injury as well as glomerulosclerosis. In the aged kidney, she demonstrated the formation of tertiary lymphoid tissues after proximal tubule injury, which cause prolonged inflammation and delayed regeneration.