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.

中文翻译：

---

巨噬细胞和破骨细胞极化的分子决定因素。


新的证据表明，巨噬细胞和破骨细胞是骨髓祖细胞的两种相互竞争的分化结果。在这篇综述中，我们总结了控制巨噬细胞和破骨细胞极化的分子机制的最新进展。这些包括核受体/转录因子，如过氧化物酶体增殖物激活受体 γ (PPARγ) 和雌激素相关受体 α (ERRα)，其转录辅因子 PPARγ 共激活剂 1-β (PGC-1β)，代谢因子，如线粒体复合物 I ( CI）成分NADH：泛醌氧化还原酶铁硫蛋白4（Ndufs4），以及跨膜受体如极低密度脂蛋白受体（VLDLR）。这些分子变阻器通过谱系内在、全身或跨代作用，促进破骨细胞分化，但抑制促炎巨噬细胞活化和炎症。这些发现为理解先天免疫与骨重塑之间的相互作用提供了新的见解，推动了骨免疫学领域的发展。