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Caveolin is a protein with a variety of functions, ranging from controlling endocytic processes to modulation of crucial signaling cascades. Thus, it is a potent regulator of diverse cellular processes. In our studies, we examine the crosstalk with TGF-β in diseased livers and investigate the functions in NAFLD/NASH with focus on metabolic alterations.
Alcohol abuse can cause chronic liver disease (e.g. cirrhosis, hepatocellular carcinoma). Upon liver damage, the pro-fibrogenic cytokine TGF-β is driving disease progression.
Hence, we are interested in clarifying the molecular crosstalk of alcohol abundance and regulations/functions of TGF-β in diseased livers. Ultimately, we aim to determine whether the TGF-β pathway could represent a novel therapeutic target in patients with alcoholic liver disease.
A crucial step in progression of hepatocellular carcinoma (HCC) is the loss of epithelial characteristics. This dedifferentiation enables cancers cells to evade the epithelial cell layer and spread to distant sites within the liver, but also to other tissue. Many transcription factors have been described to be involved in this process. Our aim is to unravel the role of novel factors on disease progression in vitro, in vivo and in human patients.