Fig. 2

The functions of LXR signaling in CNS pathology. The activation of LXR may inhibit neuroinflammation directly by transcriptional repression and indirectly by cholesterol efflux and following lysosome stabilization, which together provides a more favorable microenvironment for regeneration. The enhanced cholesterol efflux from phagocytes can also provide material for tissue repair by oligodendrocyte precursor cells (OPCs) and neural stem cells. Upregulated ApoE expression and esterification may facilitates beta-amyloid clearance. Enhanced BBB integrity and angiogenesis by LXR agonist were also documented, but the potential mechanisms remain unknown. ABC transporter ATP-binding cassette transporter, ApoE apolipoprotein E, Aβ amyloid beta, BBB blood–brain barrier, BrdU bromodeoxyuridine, COX-2 cyclooxygenase-2, eNOS endothelial nitric oxide synthase, IL-1β interleukin 1 beta, iNOS inducible nitric oxide synthase, TNFα tumor necrosis factor α