The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Osteoblast–osteoclast interactions
Open accessAbstract
Bone homeostasis depends on the resorption of bones by osteoclasts and formation of bones by the osteoblasts. Imbalance of this tightly coupled process can cause diseases such as osteoporosis. Thus, the mechanisms that regulate communication between osteoclasts and osteoblasts are critical to bone cell biology. It has been shown that osteoblasts and osteoclasts can communicate with each other through direct cell-cell contact, cytokines, and extracellular matrix interaction. Osteoblasts can affect osteoclast formation, differentiation, or apoptosis through several pathways, such as OPG/RANKL/RANK, RANKL/LGR4/RANK, Ephrin2/ephB4, and Fas/FasL pathways. Conversely, osteoclasts also influence formation of bones by osteoblasts via the d2 isoform of the vacuolar (H+) ATPase (v-ATPase) V0 domain (Atp6v0d2), complement component 3a, semaphorin 4D or microRNAs. In addition, cytokines released from the resorbed bone matrix, such as TGF-β and IGF-1, also affect the activity of osteoblasts. Drugs could be developed by enhancing or restricting some of these interactions. Several reviews have been performed on the osteoblast-osteoclast communication. However, few reviews have shown the research advances in the recent years. In this review, we summarized the current knowledge on osteoblast-osteoclast communication.
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Cites
Osteoclast differentiation and activation
Boyle, W. J., Simonet, W. S., & Lacey, D. L. (2003) · Nature · doi:10.1038/nature01658 · Cited by 6,670 · cited 4×
“progenitor cells, and activates the down signaling pathways related to cell growth and differentiation (13).”
BackgroundInfluentialFunctions of RANKL/RANK/OPG in bone modeling and remodeling
Boyce, B. F., & Xing, L. (2008) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2008.03.018 · Cited by 1,844
Yasuda, H., Shima, N., Nakagawa, N., Mochizuki, S.-I., Yano, K., Fujise, N., Sato, Y., Goto, M., Yamaguchi, K., Kuriyama, M., et al. (1998) · Endocrinology · doi:10.1210/endo.139.3.5837 · Cited by 1,201
Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST)
Balemans, W. (2001) · Human Molecular Genetics · doi:10.1093/hmg/10.5.537 · Cited by 1,147 · cited 1×
“Sclerostin is a protein that is encoded by the SOST gene in humans (52).”
BackgroundSkeletal remodeling in health and disease
Zaidi, M. (2007) · Nature Medicine · doi:10.1038/nm1593 · Cited by 1,069
Role of osteoblasts in hormonal control of bone resorption—A hypothesis
Rodan, G. A., & Martin, T. J. (1981) · Calcified Tissue International · doi:10.1007/bf02409454 · Cited by 982
Kearns, A. E., Khosla, S., & Kostenuik, P. J. (2008) · Endocrine Reviews · doi:10.1210/er.2007-0014 · Cited by 824
Osteoclast–osteoblast communication
Matsuo, K., & Irie, N. (2008) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2008.03.027 · Cited by 780
Bidirectional ephrinB2-EphB4 signaling controls bone homeostasis
Zhao, C., Irie, N., Takada, Y., Shimoda, K., Miyamoto, T., Nishiwaki, T., Suda, T., & Matsuo, K. (2006) · Cell Metabolism · doi:10.1016/j.cmet.2006.05.012 · Cited by 777
Osteoprotection by semaphorin 3A
Hayashi, M., Nakashima, T., Taniguchi, M., Kodama, T., Kumanogoh, A., & Takayanagi, H. (2012) · Nature · doi:10.1038/nature11000 · Cited by 606
Cited by
Subchondral bone microenvironment in osteoarthritis and pain
Hu, Y., Chen, X., Wang, S., Jing, Y., & Su, J. (2021) · Bone Research · doi:10.1038/s41413-021-00147-z · Cited by 577
Self-citationEstablishment and Maintenance of the Macrophage Niche
Guilliams, M., Thierry, G. R., Bonnardel, J., & Bajenoff, M. (2020) · Immunity · doi:10.1016/j.immuni.2020.02.015 · Cited by 512
Re-thinking the bone remodeling cycle mechanism and the origin of bone loss
Delaisse, J.-M., Andersen, T. L., Kristensen, H. B., Jensen, P. R., Andreasen, C. M., & Søe, K. (2020) · Bone · doi:10.1016/j.bone.2020.115628 · Cited by 152
Is osteoporosis an autoimmune mediated disorder?
Iseme, R. A., Mcevoy, M., Kelly, B., Agnew, L., Walker, F. R., & Attia, J. (2017) · Bone Reports · doi:10.1016/j.bonr.2017.10.003 · Cited by 56
Zhu, S., Häussling, V., Aspera-Werz, R. H., Chen, T., Braun, B., Weng, W., Histing, T., & Nussler, A. K. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms22010053 · Cited by 42
Stein, M., Elefteriou, F., Busse, B., Fiedler, I. A., Kwon, R. Y., Farrell, E., Ahmad, M., Ignatius, A., Grover, L., Geris, L., et al. (2023) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.4868 · Cited by 42
Deletion of Wnt5a in osteoclasts results in bone loss through decreased bone formation
Roberts, J. L., Liu, G., Paglia, D. N., Kinter, C. W., Fernandes, L. M., Lorenzo, J., Hansen, M. F., Arif, A., & Drissi, H. (2020) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.14293 · Cited by 32
Acute Myeloid Leukaemia Drives Metabolic Changes in the Bone Marrow Niche
Maynard, R. S., Hellmich, C., Bowles, K. M., & Rushworth, S. A. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.924567 · Cited by 17
Amlodipine accelerates bone healing in a stable closed femoral fracture model in mice
Department of Trauma and Reconstructive Surgery, E. K. U. T., Menger, M., Merscher, B., Scheuer, C., Braun, B., Herath, S., Rollmann, M., Stenger, D., Später, T., Pohlemann, T., et al. (2021) · European Cells and Materials · doi:10.22203/ecm.v041a38 · Cited by 16
Goodarzizadeh, N., Shahrjerdi, A., Begum, K., & Amani, R. (2026) · International Journal of Preventive Medicine · doi:10.4103/ijpvm.ijpvm_114_23
Metadata
- Authors
- Chen, X., Wang, Z., Duan, N., Zhu, G., Schwarz, E. M., & Xie, C.
- Venue
- Connective Tissue Research
- Publisher
- Informa UK Limited
- Published
- 2017-03-21
- Volume
- 59
- Issue
- 2
- Pages
- 99-107
- ISSN
- 0300-8207 (ISSN-L)
- 1607-8438
- OpenAlex
- W2586409573
- Cited by
- 873
- References
- 15
- FWCI
- 15.92
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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