Hepatitis C virus-host interactions: Etiopathogenesis and therapeutic strategies

doi:10.5493/wjem.v2.i2.7

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Apr 20, 2012 (publication date) through May 7, 2024

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World Journal of Experimental Medicine

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2220-315x

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Exp Med. Apr 20, 2012; 2(2): 7-25
Published online Apr 20, 2012. doi: 10.5493/wjem.v2.i2.7

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Figure 4 A proposed model for hepatitis C virus - mediated effects in liver cells and the modulatory role of transforming growth factor β in the regulation of both angiogenesis (A) and hepatocellular carcinoma (B). PKC: Protein kinase C; HCV: Hepatitis C virus; AP-1: Activator protein-1; CREB: cAMP response element-binding protein; JNK: c-Jun N-terminal kinase; ERK: Extracellular regulated protein kinase; TGF: Transforming growth factor; VEGF: Vascular endothelial growth factor; ROS: Reactive oxygen species; PPAR: Peroxisome proliferator-activated receptor.

Citation: Hassan M, Selimovic D, El-Khattouti A, Ghozlan H, Haikel Y, Abdelkader O. Hepatitis C virus-host interactions: Etiopathogenesis and therapeutic strategies. World J Exp Med 2012; 2(2): 7-25
URL: https://www.wjgnet.com/2220-315X/full/v2/i2/7.htm
DOI: https://dx.doi.org/10.5493/wjem.v2.i2.7