Elucidating the mechanisms of kidney fibrosis and regeneration

2016 Fiscal Year Final Research Report

• Project/Area Number: 26293202
• 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: Kyoto University
• Principal Investigator: Yanagita Motoko 京都大学, 医学(系)研究科(研究院), 教授 (70378769)
• Co-Investigator(Kenkyū-buntansha): 河本 宏 京都大学, 再生医科学研究所, 教授 (00343228)
• Co-Investigator(Renkei-kenkyūsha): OKAMOTO Hitoshi 京都大学, 薬学研究科, 教授 (60158813)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 線維化 / 再生 / 炎症 / 老化

Outline of Final Research Achievements

We demonstrated that proximal tubule injury induces the transdifferentiation of fibroblasts to myofibroblasts, and that the transdifferentiation is reversible when the proximal tubule injury is mild.
We also demonstrated that fibroblasts in aged kidney acquire the ability to produce homeostatic chemokines after injury, attract lymphocytes and trigger the formation of tertiary lymphoid tissues (TLTs). TLT formation in aged kidneys causes prolonged inflammation and delayed regeneration, and is frequently observed in aged human kidneys.

Free Research Field

腎臓内科学