The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Update on Wnt signaling in bone cell biology and bone disease
Open accessAbstract
For more than a decade, Wnt signaling pathways have been the focus of intense research activity in bone biology laboratories because of their importance in skeletal development, bone mass maintenance, and therapeutic potential for regenerative medicine. It is evident that even subtle alterations in the intensity, amplitude, location, and duration of Wnt signaling pathways affects skeletal development, as well as bone remodeling, regeneration, and repair during a lifespan. Here we review recent advances and discrepancies in how Wnt/Lrp5 signaling regulates osteoblasts and osteocytes, introduce new players in Wnt signaling pathways that have important roles in bone development, discuss emerging areas such as the role of Wnt signaling in osteoclastogenesis, and summarize progress made in translating basic studies to clinical therapeutics and diagnostics centered around inhibiting Wnt pathway antagonists, such as sclerostin, Dkk1 and Sfrp1. Emphasis is placed on the plethora of genetic studies in mouse models and genome wide association studies that reveal the requirement for and crucial roles of Wnt pathway components during skeletal development and disease.
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Cites
Polakis, P. (2000) · Genes & Development · doi:10.1101/gad.14.15.1837 · Cited by 3,183
Osteoporosis: now and the future
Rachner, T. D., Khosla, S., & Hofbauer, L. C. (2011) · The Lancet · doi:10.1016/s0140-6736(10)62349-5 · Cited by 2,696
Bonewald, L. F. (2011) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.320 · Cited by 2,287
High Bone Density Due to a Mutation in LDL-Receptor–Related Protein 5
Boyden, L. M., Mao, J., Belsky, J., Mitzner, L., Farhi, A., Mitnick, M. A., Wu, D., Insogna, K., & Lifton, R. P. (2002) · New England Journal of Medicine · doi:10.1056/nejmoa013444 · Cited by 1,591
Increased Wnt signaling during aging alters muscle stem cell fate and increases fibrosis
Brack, A. S., Conboy, M. J., Roy, S., Lee, M., Kuo, C. J., Keller, C., & Rando, T. A. (2007) · Science · doi:10.1126/science.1144090 · Cited by 1,564
Sclerostin Binds to LRP5/6 and Antagonizes Canonical Wnt Signaling
Li, X., Zhang, Y., Kang, H., Liu, W., Liu, P., Zhang, J., Harris, S. E., & Wu, D. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m413274200 · Cited by 1,366
Canonical WNT Signaling Promotes Osteogenesis by Directly Stimulating Runx2 Gene Expression
Gaur, T., Lengner, C. J., Hovhannisyan, H., Bhat, R. A., Bodine, P. V. N., Komm, B. S., Javed, A., van Wijnen, A. J., Stein, J. L., Stein, G. S., et al. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m500608200 · Cited by 1,170
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
Kato, M., Patel, M. S., Levasseur, R., Lobov, I., Chang, B. H.-J., Glass, D. A., Hartmann, C., Li, L., Hwang, T.-H., Brayton, C. F., et al. (2002) · The Journal of Cell Biology · doi:10.1083/jcb.200201089 · Cited by 1,086
Osteocytes, mechanosensing and Wnt signaling
Bonewald, L. F., & Johnson, M. L. (2008) · Bone · doi:10.1016/j.bone.2007.12.224 · Cited by 1,076
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Clevers, H., & Nusse, R. (2012) · Cell · doi:10.1016/j.cell.2012.05.012 · Cited by 5,554
Restoring Wnt/β-catenin signaling is a promising therapeutic strategy for Alzheimer’s disease
Jia, L., Piña-Crespo, J., & Li, Y. (2019) · Molecular Brain · doi:10.1186/s13041-019-0525-5 · Cited by 288
Osteoporosis: Mechanism, Molecular Target and Current Status on Drug Development
Li, H., Xiao, Z., Quarles, L. D., & Li, W. (2021) · Current Medicinal Chemistry · doi:10.2174/0929867327666200330142432 · Cited by 226
The WNT system: background and its role in bone
Lerner, U. H., & Ohlsson, C. (2015) · Journal of Internal Medicine · doi:10.1111/joim.12368 · Cited by 228
Isaac, J., Erthal, J., Gordon, J., Duverger, O., Sun, H.-W., Lichtler, A. C., Stein, G. S., Lian, J. B., & Morasso, M. I. (2014) · Cell Death & Differentiation · doi:10.1038/cdd.2014.82 · Cited by 54
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Metadata
- Authors
- Monroe, D. G., McGee-Lawrence, M. E., Oursler, M. J., & Westendorf, J. J.
- Venue
- Gene
- Publisher
- Elsevier BV
- Published
- 2012-01
- Volume
- 492
- Issue
- 1
- Pages
- 1-18
- ISSN
- 0378-1119 (ISSN-L)
- OpenAlex
- W1964059429
- Cited by
- 392
- References
- 23
- FWCI
- 15.52
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.