Liver X receptors and skeleton: Current state-of-knowledge.

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  • Author(s): Goel D;Goel D; Vohora D; Vohora D
  • Source:
    Bone [Bone] 2021 Mar; Vol. 144, pp. 115807. Date of Electronic Publication: 2020 Dec 15.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't; Review
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Elsevier Science Country of Publication: United States NLM ID: 8504048 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-2763 (Electronic) Linking ISSN: 18732763 NLM ISO Abbreviation: Bone Subsets: MEDLINE
    • Publication Information:
      Publication: New York : Elsevier Science
      Original Publication: Elmsford, NY : Pergamon Press, c1985-
    • Subject Terms:
      Bone Resorption* ; Osteoclasts*; Cell Differentiation ; Humans ; Liver X Receptors ; NF-kappa B ; NFATC Transcription Factors ; RANK Ligand ; Skeleton
    • Abstract:
      The liver X receptors (LXR) is a nuclear receptor that acts as a prominent regulator of lipid homeostasis and inflammatory response. Its therapeutic effectiveness against various diseases like Alzheimer's disease and atherosclerosis has been investigated in detail. Emerging pieces of evidence now reveal that LXR is also a crucial modulator of bone remodeling. However, the molecular mechanisms underlying the pharmacological actions of LXR on the skeleton and its role in osteoporosis are poorly understood. Therefore, in the current review, we highlight LXR and its actions through different molecular pathways modulating skeletal homeostasis. The studies described in this review propound that LXR in association with estrogen, PTH, PPARγ, RXR hedgehog, and canonical Wnt signaling regulates osteoclastogenesis and bone resorption. It regulates RANKL-induced expression of c-Fos, NFATc1, and NF-κB involved in osteoclast differentiation. Additionally, several studies suggest suppression of RANKL-induced osteoclast differentiation by synthetic LXR ligands. Given the significance of modulation of LXR in various physiological and pathological settings, our findings indicate that therapeutic targeting of LXR might potentially prevent or treat osteoporosis and improve bone quality.
      (Copyright © 2020 Elsevier Inc. All rights reserved.)
    • Contributed Indexing:
      Keywords: Liver X receptors; Nuclear receptor; Osteoporosis; RANKL
    • Accession Number:
      0 (Liver X Receptors)
      0 (NF-kappa B)
      0 (NFATC Transcription Factors)
      0 (RANK Ligand)
    • Publication Date:
      Date Created: 20201217 Date Completed: 20210705 Latest Revision: 20210705
    • Publication Date:
      20240829
    • Accession Number:
      10.1016/j.bone.2020.115807
    • Accession Number:
      33333244