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. Author manuscript; available in PMC: 2012 Nov 1.
Published in final edited form as: Gastroenterology. 2011 Sep 12;141(5):1572–1585. doi: 10.1053/j.gastro.2011.09.002

Figure 4.

Figure 4

Mechanisms of liver fibrosis in patients with ALD. (1) Alcohol consumption causes hepatocyte damage, which leads to the release of a variety of mediators and the subsequent induction of stellate cell activation. (2) Acetaldehyde directly targets stellate cells and up-regulates the expression of collagens in these cells. (3) Alcohol consumption results in elevation of LPS levels in the liver. LPS can directly enhance stellate cell activation via up-regulation of TGF-β signaling and indirectly promote stellate cell activation via activation of Kupffer cells to release profibrotic cytokines and chemokines. (4) Natural killer (NK) cells are activated during viral hepatitis or IFN-α therapy. Activated natural killer cells can kill stellate cells by releasing TRAIL and inhibit stellate cell proliferation by releasing IFN-γ; they therefore have an important role in inhibiting liver fibrosis. Alcohol consumption suppresses the antifibrotic effects of NK cells and IFN-γ, thereby promoting liver fibrosis.