Molecular determinants for the polarization of macrophage and osteoclast

Dengbao Yang, Yihong Wan

Research output: Contribution to journalReview article

Abstract

Emerging evidence suggest that macrophage and osteoclast are two competing differentiation outcomes from myeloid progenitors. In this review, we summarize recent advances in the understanding of the molecular mechanisms controlling the polarization of macrophage and osteoclast. These include nuclear receptors/transcription factors such as peroxisome proliferator-activated receptor γ (PPARγ) and estrogen-related receptor α (ERRα), their transcription cofactor PPARγ coactivator 1-β (PGC-1β), metabolic factors such as mitochondrial complex I (CI) component NADH:ubiquinone oxidoreductase iron-sulfur protein 4 (Ndufs4), as well as transmembrane receptors such as very-low-density-lipoprotein receptor (VLDLR). These molecular rheostats promote osteoclast differentiation but suppress proinflammatory macrophage activation and inflammation, by acting lineage-intrinsically, systemically or cross generation. These findings provide new insights to the understanding of the interactions between innate immunity and bone remodeling, advancing the field of osteoimmunology.

Original languageEnglish (US)
Pages (from-to)551-563
Number of pages13
JournalSeminars in Immunopathology
Volume41
Issue number5
DOIs
StatePublished - Sep 1 2019

Fingerprint

Osteoclasts
Peroxisome Proliferator-Activated Receptors
Macrophages
Iron-Sulfur Proteins
Electron Transport Complex I
Macrophage Activation
Bone Remodeling
Cytoplasmic and Nuclear Receptors
Innate Immunity
Estrogen Receptors
Transcription Factors
Inflammation

Keywords

  • Bone
  • ERRα
  • Macrophage
  • Ndufs4
  • Osteoclast
  • Osteoimmunology
  • PGC-1β
  • PPARγ
  • VLDLR

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Molecular determinants for the polarization of macrophage and osteoclast. / Yang, Dengbao; Wan, Yihong.

In: Seminars in Immunopathology, Vol. 41, No. 5, 01.09.2019, p. 551-563.

Research output: Contribution to journalReview article

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