Soluble Endoglin modulates TGF-β1 mediated signaling in isolated hepatocytes
Article 2008 de
Authors
SM
SK Meurer
MR
MS Rizk
LT
Lidia Tihaa
Abstract
1 min read
Aims: Hepatocellular carcinoma (HCC) is one of the most frequent tumors worldwide. The incidence to develop HCC in patients with fibrosis or even cirrhosis is high. Transforming growth factor-β (TGF-β) is a key cytokine in the process of fibrogenesis. We have previously shown that the soluble part of Endoglin, a type III TGF-β receptor, is upregulated in late stages of fibrosis and cirrhosis [1]. To evaluate the physiological consequences we analyzed the functional impact of the heterologously expressed soluble endoglin on TGF-β/Smad3 signaling.
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