Dr. Wilhelm Kriz and colleagues at the University of Heidelberg, Heidelberg, Germany; the University of Paris, Paris, France; the University of Zurich, Zurich, Switzerland; the University of Berlin, Berlin, Germany; the University of Leipzig, Leipzig, Germany; and the Pennsylvania State University, University Park, Pennsylvania demonstrate that TGF-β1 contributes to kidney disease.
Their report can be found in the August 2010 issue of the American Journal of Pathology.
Chronic kidney disease and end stage renal disease affect more than 2 out of every 1,000 people in the United States. Diabetes and high blood pressure are the two most common causes of chronic kidney disease.
Fibrosis in the kidney is one of the key causes of progressive renal failure. High levels of the inflammatory molecule TGF-β1 in the kidney tubules due to tissue damage can cause fibrosis as well as nephron degeneration, resulting in loss of kidney function. To clarify the mechanisms regulating TGF-β1-mediated renal fibrosis, Koesters et al expressed high levels of TGF-β1 in renal tubules of mice. Nephron degeneration in this system was mediated by decomposition of the tubular cells. These data suggest that TGF-β1 may play a novel role in cell death of renal cells, thus contributing to renal fibrosis.
Dr. Kriz's group "uncover[ed] a novel potential role of TGF-β1, i.e. the induction of autophagy in renal epithelial cells. Its relevance under more usual pathological conditions as a possible further mechanism of programmed cell death remains to be established."
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