Del Fattore Andrea, Teti Anna, Rucci Nadia
Department of Experimental Medicine, University of L'Aquila, Via Vetoio, Coppito 2, 67100 L'Aquila, Italy.
Arch Biochem Biophys. 2008 May 15;473(2):147-60. doi: 10.1016/j.abb.2008.01.011. Epub 2008 Jan 24.
Osteoclasts are bone-resorbing cells derived from hematopoietic precursors of the monocyte-macrophage lineage. Besides the well known Receptor Activator of Nuclear factor-kappaB (RANK), RANK ligand and osteoprotegerin axis, a variety of factors tightly regulate osteoclast formation, adhesion, polarization, motility, resorbing activity and life span, maintaining bone resorption within physiological ranges. Receptor-mediated osteoclast regulation is rather complex. Nuclear receptors, cell surface receptors, integrin receptors and cell death receptors work together to control osteoclast activity and prevent both reduced or increased bone resorption. Here we will discuss the signal transduction pathways activated by the main osteoclast receptors, integrating their function and mechanisms of action.
破骨细胞是源自单核细胞-巨噬细胞谱系造血前体的骨吸收细胞。除了众所周知的核因子κB受体激活剂(RANK)、RANK配体和骨保护素轴外,多种因素严格调节破骨细胞的形成、黏附、极化、运动、吸收活性和寿命,将骨吸收维持在生理范围内。受体介导的破骨细胞调节相当复杂。核受体、细胞表面受体、整合素受体和细胞死亡受体共同作用以控制破骨细胞活性,并防止骨吸收减少或增加。在此,我们将讨论主要破骨细胞受体激活的信号转导途径,整合它们的功能和作用机制。