Abstract
Cystic diseases of the kidney (CDK) with consecutive interstitial fibrosis represent the most frequent hereditary causes of end-stage renal failure in children and adults. Up to now no causal treatment for any of them is available in humans. It is shown that the TGF-β pathway is playing a major role in the development of interstitial fibrosis and an overexpression of Smad7, the negative inhibitor of TGF-β, is able to prevent fibrosis. Therefore we want to analyse the effect of a long term expression of Smad7 on renal function and interstitial fibrosis in our CDK animal models.
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