September 13, 2011
From left: Mr. Masayuki Takase, Graduate school of
Medicine, Associate Professor Motoko Yanagita,
The Hakubi Center and Dr. Nariaki Asada, Kyoto
University Hospital
Applicable to chronic kidney disease drug development
Chronic kidney disease is a worldwide public health problem. Associate Professor Motoko Yanagita and her research team have elucidated the mechanisms of common complications in the progressive stages of chronic kidney disease; renal fibrosis and renal anemia.
Renal fibrosis is the consequence of an excessive production of extracellular matrix produced by scar-producing cells, whereas renal anemia is mediated by the reduced production of erythropoietin (EPO), an erythrocyte production–stimulating hormone in the injured kidney.
Associate Professor Yanagita and her team demonstrated that EPO-producing cells in healthy kidneys and scar-producing cells during fibrosis both originate from a single cell lineage with neural characteristics. These cells enter the developing kidney during embryogenesis, and transform from one to the other depending on the status of the kidney. They further demonstrated that renal anemia is caused by the loss of EPO production in this cell lineage during fibrosis, and more importantly, that this loss can be restored in vivo. The discovery of the reversibility of reduced EPO production and fibrosis leads to the possibility of better therapeutic approaches for treating chronic kidney disease in the near future.
Link to the Journal paper:
http://dx.doi.org/10.1172/JCI57301
http://hdl.handle.net/2433/147049 （Research Information Repository KURENAI）
Asada N, Takase M, Nakamura J, Oguchi A, Asada M, Suzuki N, Yamamura K, Nagoshi N, Shibata S, Rao TN, Fehling HJ, Fukatsu A, Minegishi N,8, Kita T, Kimura T, Okano H, Yamamoto M, Yanagita M. Dysfunction of fibroblasts of extrarenal origin underlies renal fibrosis and renal anemia in mice.
J Clin Invest. 2011; doi:10.1172/JCI57301; Published September 12, 2011.