Exploring Molecular Mechanisms of Liver Fibrosis

Dear Colleagues,

Fibrosis is a double-edged sword. On the one hand, it can be the final state of a healed inflammation as scar tissue; on the other hand, it is frequently associated with a reduction or loss of organ function. Moreover, especially in liver disease, it is a surrogate parameter that indicates a progression of the disease to liver cirrhosis or even hepatocellular carcinoma. This is especially true for non-alcoholic fatty liver disease, a pandemic disorder associated with Western lifestyles and diets. To influence organ fibrosis, it is important to better understand its induction, perpetuation and termination at the molecular level. The induction of liver fibrosis may be metabolic (e.g. alcohol, diet, drugs), infectious (e.g. viruses), autoimmune (e.g. primary biliary cholangitis) or due to monogenetic defects (e.g. increased iron storage). The molecular mechanisms on the way to the final stage fibrosis are very different – dependent on its pathogenesis. It is the aim of this special issue to provide more insight into these processes.

Prof. Dr. Tilman Sauerbruch
Prof. Dr. Ralf Weiskirchen
Guest Editors

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