Targeting gut flora to prevent progression of hepatocellular carcinoma

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Targeting gut flora to prevent progression of hepatocellular carcinoma Marion Darnaud, Jamila Faivre, Nicolas Moniaux  Journal of Hepatology  Volume 58, Issue 2, Pages 385-387 (February 2013) DOI: 10.1016/j.jhep.2012.08.019 Copyright © 2012 European Association for the Study of the Liver Terms and Conditions

Fig. 1 Hypothetic diagram of HCC promotion by the LPS/TLR4 pathway. The progression of HCC depends on the balance between TRL4-induced proliferative, pro-survival, and apoptotic signals in chronically injured hepatocytes. The chronic inflamed liver is associated with intestinal dysbiosis, gut permeability changes, and PAMP (LPS) translocation to the liver. The TLR4 signaling is activated by LPS in hepatic stellate cells and hepatocytes, resulting in extracellular matrix (ECM) remodeling, fibrogenesis, and secretion of the epiregulin growth factor, which triggers tumor hepatocyte proliferation. The inflammatory liver signals to the gut, maintaining, or amplifying, intestinal dysbiosis. Journal of Hepatology 2013 58, 385-387DOI: (10.1016/j.jhep.2012.08.019) Copyright © 2012 European Association for the Study of the Liver Terms and Conditions