Activation of liver X receptors inhibits experimental fibrosis by interfering with interleukin-6 release from macrophages

    March 2014 in “ Annals of the Rheumatic Diseases ”
    Christian Beyer, Jingang Huang, Jürgen Beer, Yun Zhang, Katrin Palumbo‐Zerr, Pawel Zerr, Alfiya Distler, Clara Dees, Christiane Maier, Luis E. Muñoz, Gerhard Krönke, Stefan Uderhardt, Oliver Distler, Simon A. Jones, Stefan Rose‐John, Tamás Oravecz, Georg Schett, Jörg H. W. Distler
    The study investigated the role of liver X receptors (LXRs) in experimental skin fibrosis and evaluated their potential as antifibrotic targets. It was found that activation of LXRs by the agonist T0901317 had antifibrotic effects in various models of fibrotic disease, particularly in inflammation-driven models like bleomycin-induced skin fibrosis and sclerodermatous graft-versus-host disease (sclGvHD). The antifibrotic effects were not due to direct action on fibroblasts but rather through the inhibition of macrophage infiltration and their release of the pro-fibrotic interleukin-6. This suggested that LXRs could be novel targets for antifibrotic therapies, especially in patients with inflammatory disease subtypes.
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