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Nature Communications

March 14, 2012

The loss of inhibitory proteins in a type of cell known as fibroblasts is associated with fibrotic diseases, reports a paper published in Nature Communications this week. The finding could eventually prove useful in the development of specific treatments for fibrosis. In fibrotic diseases, such as pulmonary fibrosis or liver cirrhosis, an overproduction of springy molecules, like collagen, by fibroblasts can disrupt the function of tissues and organs. The molecular mechanisms leading to the unusual activation of fibroblasts are incompletely understood, which has hindered the development of anti-fibrotic therapies. Studying skin sections from patients with various fibrotic diseases, Jorg Distler and his team found that the protein Dickkopf-1 was missing in fibroblasts in fibrotic skin. They noted that mice that produced Dickkopf-1 continuously were protected from fibrosis in various experimental models of the disease. The group show that loss of Dickkopf-1 is caused by a growth factor that is known to be involved in fibrosis, and that Dickkopf-1 normally inhibits the signalling molecule Wnt. The findings suggest that inhibition of Wnt signalling by Dickkopf-1 or specific drugs might be an effective treatment of fibrotic diseases.

DOI:10.1038/ncomms1734 | Original article

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