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JCI online early table of contents: Oct. 18, 2010
Date:10/18/2010

>Chronic kidney disease is the ninth leading cause of death in the United States. It is the term given to the progressive loss of kidney function over many months or years culminating in end-stage renal disease, which requires treatment with dialysis or a kidney transplant. A team of researchers, led by Katalin Susztak, at Albert Einstein College of Medicine, New York, has now generated new data, by analysis of a mouse model of chronic kidney disease and kidney samples from patients with the condition, that lead them to suggest that inhibiting activation of the Notch signaling pathway might provide a way to reduce progression to end-stage renal disease.

TITLE: Epithelial Notch signaling regulates interstitial fibrosis development in the kidneys of mice and humans

AUTHOR CONTACT:
Katalin Susztak
Albert Einstein College of Medicine, New York, New York, USA.
Phone: 718.430.3498; Fax: 718.430.8963; E-mail: katalin.susztak@einstein.yu.edu.

View this article at: http://www.jci.org/articles/view/43025?key=57c3da7d127adbe6b9ab


HEPATOLOGY: Ameliorating scarring of the liver

Chronic liver damage, such as that caused by chronic infection with hepatitis C virus or by chronic alcohol abuse, leads to scarring of the liver tissue (a condition also known as liver fibrosis) and ultimately end-stage liver disease. A team of researchers, led by Hermann Wasmuth, at University Hospital Aachen, Germany, has now found a way to ameliorate experimental liver fibrosis in mice. Specifically, the team found that an antagonist of the proteins to which the molecule Ccl5 binds ameliorated liver fibrosis in two mouse models of the condition and was able to accelerate fibrosis regression. These results are likely to have clinical implications because in patients with liver fibrosis, high levels
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Contact: Karen Honey
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Journal of Clinical Investigation
Source:Eurekalert

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