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A deer in the headlights: BAMBI meets liver fibrosis

Nature Medicine volume 13, pages 1281–1282 (2007)Cite this article

Lipopolysaccharide signaling through the Toll-like receptors downregulates an inhibitory pseudoreceptor of TGF-β, enhancing hepatic fibrosis and liver injury (pages 1324–1332).

Chronic liver disease leads to continual injury and a wound-healing response in the organ, which causes a torrent of problems. The injuries contribute to a cascade of events in which gut bacteria leak from the intestine, provoking the recruitment of inflammatory cells, which drown the microenvironment in fibrogenic cytokines. In a misguided damage-control response to these threats, resident mesenchymal cells, or stellate cells, generate a scar (fibrosis) that over time can obstruct blood flow and compromise hepatic function, leading to liver failure. Activation of innate immunity, specifically of Toll-like receptor (TLR) signaling, has emerged as a central component of the liver's inflammatory response to gut bacteria, but it has been unclear whether and how TLR activity amplifies the fibrogenic response of liver.

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Figure 1: Fibrogenic signaling induced by TLR4 in hepatic stellate cells and the role of Kupffer cells.

Kim Caesar

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Authors and Affiliations

  1. Scott L. Friedman is in the Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, Box 1123, 1425 Madison Ave., Room 1170C, New York, New York 10029-6574, USA. scott.friedman@mssm.edu,

    Scott L Friedman

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  1. Scott L Friedman
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Friedman, S. A deer in the headlights: BAMBI meets liver fibrosis. Nat Med 13, 1281–1282 (2007). https://doi.org/10.1038/nm1107-1281

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