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JCI online early table of contents: Sept. 12, 2011
Date:9/12/2011

on, Massachusetts, USA.
Phone: 617.724.8922; Fax: 617.726.5669; E-mail: ssever@partners.org.

Jochen Reiser
University of Miami, Miami, Florida, USA.
Phone: 305.243.2349; Fax: 305.243.2309; E-mail: jreiser@med.miami.edu.

View this article at: http://www.jci.org/articles/view/58552?key=b618f54191c2ab2d5ed1


NEPHROLOGY: Cells from outside the kidney link two features of chronic kidney disease

Individuals with chronic kidney disease often suffer from anemia. This is because the cells in the kidney that produce erythropoietin, the hormone that stimulates the production of new red blood cells in the bone marrow, are dysfunctional in these individuals. Dysfunction of these cells (fibroblasts) also causes scarring of the kidney, a condition known as renal fibrosis, which is a central feature of chronic kidney disease. Despite the importance of fibroblasts in chronic kidney disease, little is known about their origin and how they are regulated. Now, a team of researchers, led by Motoko Yanagita, at Kyoto University, Japan, has determined that the majority of erythropoietin-producing fibroblasts in the healthy mouse kidney are derived from cells that originally came from outside the kidney. Importantly, in the diseased kidney, these particular fibroblasts became dysfunctional, decreasing production of erythropoietin and contributing to fibrosis. Further, in a mouse model of renal fibrosis, treatment with tamoxifen (a drug FDA approved to treat breast cancer) increased erythropoietin production and decreased fibrosis. The authors therefore suggest that tamoxifen and related drugs could provide benefit to individuals with chronic kidney disease.

TITLE: Dysfunction of fibroblasts of extrarenal origin underlies renal fibrosis and renal anemia
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