Osteoclast differentiation and activation

By W. J. Boyle, W. S. Simonet, D. Lacey. Nature, 2003

6,592 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/54d0959e03fb5120b1fce491a85c87f1e8cc04a9

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Citations in the corpus

From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation (2014, background): “Excessive bone loss mediated by osteoclasts plays a major role in certain pathologic conditions, such as rheumatoid arthritis (RA) and osteoporosis (67, 68).”
The molecular triad OPG/RANK/RANKL: involvement in the orchestration of pathophysiological bone remodeling. (2004, background): “Moreover, the phosphatidyl-inositol-30-kinase (PI3K)/Akt pathways, which involve the mammalian target of rapamycin (mTOR) [110,111], are also targets of TRAF6.”
Degenerative Disorders of the Temporomandibular Joint: Etiology, Diagnosis, and Treatment (2008, background): “Of these cytokines, tumor necrosis factor- and interleukin1 and -6, produced primarily by stimulated macrophages, play crucial roles in the pathogenesis of rheumatoid arthritis and osteoarthrosis, with respect to the acceleration and progression of cartilage degradation, because they promote bone re”
The aging of Wolff's "law": ontogeny and responses to mechanical loading in cortical bone. (2004, background): “Stimulators include PTH, 1,25(OH)2 vitamin D3, thyroid hormone, glucocorticoids, IGF-I, and BMP-2 and -4; inhibitors include calcitonin, nitric oxide (NO), gonadal steroids, and interleukin-1 and -6 (Jee, 2001; Boyle et al., 2003).”
Tissue-specific signals control reversible program of localization and functional polarization of macrophages. (2014, neutral): “However, with some exceptions (Boyle et al., 2003), these signals remain largely unknown.”
Normal bone anatomy and physiology. (2008, background): “H ions acidify the resorption compartment beneath osteoclasts to dissolve the mineral component of bone matrix, whereas cathepsin K digests the proteinaceous matrix, which is mostly composed of type I collagen (11).”
Transforming Growth Factor- 1 to the Bone (2005, background): “Runx2 binding sites are found in the promoters of several bone formation markers including collagen 1, ALP, osteopontin, RANKL, and osteocalcin (149).”
Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis (2004, background): “Receptor activator of NF-κB ligand (RANKL) regulates the differentiation of bone-resorbing cells, osteoclasts, in the presence of macrophage-colony stimulating factor (M-CSF”
Cancer metastasis: building a framework. (2006, background): “Osteoclasts, derived from the monocytic branch of hematopoiesis, can be differentiated and stimulated through the expression of cytokines, including M-CSF, RANKL, IL-6, IL-8, and IL-11 (Boyle et al., 2003).”
Osteoblast-Osteoclast Communication and Bone Homeostasis (2020, background): “OPG is considered to function as a decoy receptor binding to RANKL, negatively regulating osteoclast differentiation and activation by blocking the RANKL-RANK interaction [6,57].”
Functional plasticity of macrophages: reversible adaptation to changing microenvironments (2004, background): “Trance (receptor activator of nuclear factor- B ligand) is a potent inducer of osteoclastogenesis [24] and apparently, also the interesting synergistic pairing of TNF- and TGF- [25].”
Osteoblast-Osteoclast Interactions (2017, background): “progenitor cells, and activates the down signaling pathways related to cell growth and differentiation (13).”
Inflammation, Fracture and Bone Repair (2016, background): “Crosstalk between inflammator bone matrix through acidic decalcification and proteolytic dissolution [76].”
Osteoimmunology: interplay between the immune system and bone metabolism. (2006, background): “Many well-known osteotropic factors, including IL-1, IL-6, and IL-11, are now believed to exert most of their osteoclastogenic activity by inducing TRANCE expression on OBs (60, 64).”