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Comment
. 2012 Sep 4;109(36):14293-4.
doi: 10.1073/pnas.1212048109. Epub 2012 Aug 27.

Fueling fibrosis in chronic hepatitis C

Ramon Bataller  1 , Stanley M Lemon
Affiliations
Comment

Fueling fibrosis in chronic hepatitis C

Ramon Bataller et al. Proc Natl Acad Sci U S A. .
No abstract available

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Fig. 1.
Fig. 1.
Mechanisms of HCV-associated liver fibrosis. HCV replicates primarily (possibly exclusively) in hepatocytes, but infects only a small minority of these cells. The viral E1 and E2 envelope proteins, and viral peptides presented with HLA molecules, elicit B- and T-cell host immune responses. Neutralizing antibodies bind to HVR1 and elsewhere on E2, driving evolution of the viral sequence. Immune cells, including T cells and monocytes, are recruited to the infected liver, secreting inflammatory mediators such as MCP-1 and RANTES. HCV proteins induce mitochondrial damage and subsequent formation of ROS in hepatocytes. Resident macrophages (Kupffer cells) are activated, and also secrete inflammatory and fibrogenic mediators. Cytokines and chemokines together with ROS activate HSCs, inducing their transformation into myofibroblasts. These cells in turn secrete proinflammatory mediators, including MCP-1, that further stimulate the recruitment of immune cells, thereby amplifying the inflammatory reaction. Myofibroblasts produce large amounts of collagen and slow matrix degradation, leading to tissue fibrosis. These processes are significantly accelerated by cofactors such as alcohol.
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Comment on

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