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. Author manuscript; available in PMC: 2012 Mar 6.
Published in final edited form as: Nat Rev Gastroenterol Hepatol. 2011 Feb;8(2):108–118. doi: 10.1038/nrgastro.2010.213

Figure 2.

Figure 2

The contribution of NF-κB to hepatic stellate cell activation and survival. LPS activates TLR4 on quiescent HSCs to downregulate the inhibitory TGFβ pseudoreceptor BAMBI, and to increase chemotaxis of Kupffer cells in an NF-κB-dependent manner. Recruited Kupffer cells then release TGFβ, which activates HSCs in an unrestricted manner owing to low levels of BAMBI. Once HSCs have become activated, NF-κB plays an additional important role by enhancing their survival. The NF-κB activation in activated hepatic stellate cells is mediated by LPS, mediators released from Kupffer cells (such as IL-1β and TNF) and angiotensin II, which is released and acts on HSCs in an autocrine manner. Together, the increased activation and survival of HSCs result in increased numbers of activated HSCs in the liver and increased deposition of extracellular matrix. Abbreviations: AngII, angiotensin II; HSC, hepatic stellate cell; IL-1, interleukin 1; LPS, lipopolysaccharide; NF-κB, nuclear factor κB; TLR4, Toll-like receptor 4; TGFβ, transforming growth factor β, TGFβR1, transforming growth factor β receptor 1; TNF, tumor necrosis factor.