Dear Colleagues,

Fibrosis is a double-edged sword. On the one hand, it can be the final state of healed inflammation as scar tissue; on the other hand, it is frequently associated with a reduction in or loss of organ function. Moreover, especially in liver disease, it is a surrogate parameter that indicates the 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 and drugs), infectious (e.g., viruses), autoimmune (e.g., primary biliary cholangitis) or due to monogenetic defects (e.g., increased iron storage). The molecular mechanisms leading to 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. Ralf Weiskirchen
Prof. Dr. Tilman Sauerbruch
Guest Editors

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• fibrosis
• hepatic stellate cells
• portal hypertension
• extracellular matrix
• cytokines
• chemokines
• biomarkers
• NASH
• NAFLD
• cirrhosis
• hepatocellular carcinoma
• therapy
• animal models
• imaging of hepatic fibrosis
• biomarkers of hepatic fibrosis