The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Sclerostin and Dickkopf-1 as Therapeutic Targets in Bone Diseases
Abstract
The processes of bone growth, modeling, and remodeling determine the structure, mass, and biomechanical properties of the skeleton. Dysregulated bone resorption or bone formation may lead to metabolic bone diseases. The Wnt pathway plays an important role in bone formation and regeneration, and expression of two Wnt pathway inhibitors, sclerostin and Dickkopf-1 (DKK1), appears to be associated with changes in bone mass. Inactivation of sclerostin leads to substantially increased bone mass in humans and in genetically manipulated animals. Studies in various animal models of bone disease have shown that inhibition of sclerostin using a monoclonal antibody (Scl-Ab) increases bone formation, density, and strength. Additional studies show that Scl-Ab improves bone healing in models of bone repair. Inhibition of DKK1 by monoclonal antibody (DKK1-Ab) stimulates bone formation in younger animals and to a lesser extent in adult animals and enhances fracture healing. Thus, sclerostin and DKK1 are emerging as the leading new targets for anabolic therapies to treat bone diseases such as osteoporosis and for bone repair. Clinical trials are ongoing to evaluate the effects of Scl-Ab and DKK1-Ab in humans for the treatment of bone loss and for bone repair.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
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
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
Self-citationMechanical Stimulation of Bone in Vivo Reduces Osteocyte Expression of Sost/Sclerostin
Robling, A. G., Niziolek, P. J., Baldridge, L. A., Condon, K. W., Allen, M. R., Alam, I., Mantila, S. M., Gluhak-Heinrich, J., Bellido, T. M., Harris, S. E., et al. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m705092200 · Cited by 1,350
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
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
Kremen proteins are Dickkopf receptors that regulate Wnt/β-catenin signalling
Mao, B., Wu, W., Davidson, G., Marhold, J., Li, M., Mechler, B. M., Delius, H., Hoppe, D., Stannek, P., Walter, C., et al. (2002) · Nature · doi:10.1038/nature756 · Cited by 1,038
Brunkow, M. E., Gardner, J. C., Van Ness, J., Paeper, B. W., Kovacevich, B. R., Proll, S., Skonier, J. E., Zhao, L., Sabo, P. J., Fu, Y.-H., et al. (2001) · The American Journal of Human Genetics · doi:10.1086/318811 · Cited by 1,011
Sclerostin is a delayed secreted product of osteocytes that inhibits bone formation
Poole, K. E. S., Van Bezooijen, R. L., Loveridge, N., Hamersma, H., Papapoulos, S. E., Löwik, C. W., & Reeve, J. (2005) · The FASEB Journal · doi:10.1096/fj.05-4221fje · Cited by 965
Cited by
Romosozumab in Postmenopausal Women with Low Bone Mineral Density
McClung, M. R., Grauer, A., Boonen, S., Bolognese, M. A., Brown, J. P., Diez-Perez, A., Langdahl, B. L., Reginster, J.-Y., Zanchetta, J. R., Wasserman, S. M., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1305224 · Cited by 1,258
Sex Steroid Actions in Male Bone
Vanderschueren, D., Laurent, M. R., Claessens, F., Gielen, E., Lagerquist, M. K., Vandenput, L., Börjesson, A. E., & Ohlsson, C. (2014) · Endocrine Reviews · doi:10.1210/er.2014-1024 · Cited by 327
Ominsky, M. S., Niu, Q.-T., Li, C., Li, X., & Ke, H. Z. (2014) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.2152 · Cited by 167
Self-citationTaylor, S., Ominsky, M. S., Hu, R., Pacheco, E., He, Y. D., Brown, D. L., Aguirre, J. I., Wronski, T. J., Buntich, S., Afshari, C. A., et al. (2016) · Bone · doi:10.1016/j.bone.2015.12.013 · Cited by 106
Self-citationImpact of Phosphorus-Based Food Additives on Bone and Mineral Metabolism
Gutiérrez, O. M., Luzuriaga-McPherson, A., Lin, Y., Gilbert, L. C., Ha, S.-W., & Beck, G. R. (2015) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2015-2279 · Cited by 82
Future directions for new medical entities in osteoporosis
Ferrari, S. (2014) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/j.beem.2014.08.002 · Cited by 34
Metadata
- Authors
- Ke, H. Z., Richards, W. G., Li, X., & Ominsky, M. S.
- Venue
- Endocrine Reviews
- Publisher
- The Endocrine Society
- Published
- 2012-06-20
- Volume
- 33
- Issue
- 5
- Pages
- 747-783
- ISSN
- 0163-769X (ISSN-L)
- 1945-7189
- OpenAlex
- W2118492754
- Cited by
- 402
- References
- 16
- FWCI
- 38.56
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
Data sources
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.
