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
    TLDR Activating liver X receptors can reduce fibrosis by stopping certain immune cells from releasing harmful proteins.
    The study investigated the role of liver X receptors (LXRs) in experimental skin fibrosis and evaluated their potential as antifibrotic targets. Activation of LXRs by the agonist T0901317 demonstrated antifibrotic effects in models of bleomycin-induced skin fibrosis, sclerodermatous graft-versus-host disease (sclGvHD), and tight skin-1 (Tsk-1) mice. The antifibrotic activity was particularly notable in inflammation-driven models. LXR activation inhibited fibrosis by interfering with macrophage infiltration and their release of the pro-fibrotic interleukin-6, rather than directly targeting fibroblasts. The study concluded that LXRs could be novel targets for antifibrotic therapies, especially in patients with inflammatory disease subtypes.
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