The DOI matches its Crossref record; 251 of the 251 references it cites were found in a registry or an index.
Role of FGF/FGFR signaling in skeletal development and homeostasis: learning from mouse models
Open accessAbstract
Fibroblast growth factor (FGF)/fibroblast growth factor receptor (FGFR) signaling plays essential roles in bone development and diseases. Missense mutations in FGFs and FGFRs in humans can cause various congenital bone diseases, including chondrodysplasia syndromes, craniosynostosis syndromes and syndromes with dysregulated phosphate metabolism. FGF/FGFR signaling is also an important pathway involved in the maintenance of adult bone homeostasis. Multiple kinds of mouse models, mimicking human skeleton diseases caused by missense mutations in FGFs and FGFRs, have been established by knock-in/out and transgenic technologies. These genetically modified mice provide good models for studying the role of FGF/FGFR signaling in skeleton development and homeostasis. In this review, we summarize the mouse models of FGF signaling-related skeleton diseases and recent progresses regarding the molecular mechanisms, underlying the role of FGFs/FGFRs in the regulation of bone development and homeostasis. This review also provides a perspective view on future works to explore the roles of FGF signaling in skeletal development and homeostasis. Mouse models are revealing new insights into the roles of fibroblast growth factor (FGF) in human bone development and skeletal diseases. In a review article, Lin Chen and colleagues from the Third Military Medical University in Chongqing, China, highlight the many essential roles that FGFs, a family of growth factors, and their receptors play in the formation of a healthy skeleton. Mutations in FGF-associated genes can cause a range of congenital bone disorders. The authors discuss the ways in which scientists are genetically engineering mice to harbor mutations in a range of genes coding for FGFs and their receptors. These animal models are offering a window into the molecular mechanisms that underlie genetic skeletal diseases and providing attractive drug targets for treating many bone-related disorders.
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
Ahmed, A., Jorna, T., & Bhandari, S. (2016) · Nephron · doi:10.1159/000447068 · Cited by 11,717
Identification of the haematopoietic stem cell niche and control of the niche size
Zhang, J., Niu, C., Ye, L., Huang, H., He, X., Tong, W.-G., Ross, J., Haug, J., Johnson, T., Feng, J. Q., et al. (2003) · Nature · doi:10.1038/nature02041 · Cited by 2,959
FGF-21 as a novel metabolic regulator
Kharitonenkov, A., Shiyanova, T. L., Koester, A., Ford, A. M., Micanovic, R., Galbreath, E. J., Sandusky, G. E., Hammond, L. J., Moyers, J. S., Owens, R. A., et al. (2005) · Journal of Clinical Investigation · doi:10.1172/jci23606 · Cited by 2,125
FGF23 induces left ventricular hypertrophy
Faul, C., Amaral, A. P., Oskouei, B., Hu, M.-C., Sloan, A., Isakova, T., Gutiérrez, O. M., Aguillon-Prada, R., Lincoln, J., Hare, J. M., et al. (2011) · Journal of Clinical Investigation · doi:10.1172/jci46122 · Cited by 2,027
Cellular signaling by fibroblast growth factor receptors
Eswarakumar, V. P., Lax, I., & Schlessinger, J. (2005) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2005.01.001 · Cited by 1,929
FGF-23 Is a Potent Regulator of Vitamin D Metabolism and Phosphate Homeostasis
Shimada, T., Hasegawa, H., Yamazaki, Y., Muto, T., Hino, R., Takeuchi, Y., Fujita, T., Nakahara, K., Fukumoto, S., & Yamashita, T. (2004) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.0301264 · Cited by 1,883
Receptor Specificity of the Fibroblast Growth Factor Family
Ornitz, D. M., Xu, J., Colvin, J. S., McEwen, D. G., MacArthur, C. A., Coulier, F., Gao, G., & Goldfarb, M. (1996) · Journal of Biological Chemistry · doi:10.1074/jbc.271.25.15292 · Cited by 1,871
Fibroblast growth factor 15 functions as an enterohepatic signal to regulate bile acid homeostasis
Inagaki, T., Choi, M., Moschetta, A., Peng, L., Cummins, C. L., McDonald, J. G., Luo, G., Jones, S. A., Goodwin, B., Richardson, J. A., et al. (2005) · Cell Metabolism · doi:10.1016/j.cmet.2005.09.001 · Cited by 1,865
Reaching a Genetic and Molecular Understanding of Skeletal Development
Karsenty, G., & Wagner, E. F. (2002) · Developmental Cell · doi:10.1016/s1534-5807(02)00157-0 · Cited by 1,601
Shimada, T., Kakitani, M., Yamazaki, Y., Hasegawa, H., Takeuchi, Y., Fujita, T., Fukumoto, S., Tomizuka, K., & Yamashita, T. (2004) · Journal of Clinical Investigation · doi:10.1172/jci19081 · Cited by 1,596
Cited by
FGF/FGFR signaling in health and disease
Xie, Y., Su, N., Yang, J., Tan, Q., Huang, S., Jin, M., Ni, Z., Zhang, B., Zhang, D., Luo, F., et al. (2020) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-020-00222-7 · Cited by 904
Self-citationMolecular mechanosensors in osteocytes
Qin, L., Liu, W., Cao, H., & Xiao, G. (2020) · Bone Research · doi:10.1038/s41413-020-0099-y · Cited by 484
A Sprouty4 reporter to monitor FGF/ERK signaling activity in ESCs and mice
Morgani, S. M., Saiz, N., Garg, V., Raina, D., Simon, C. S., Kang, M., Arias, A. M., Nichols, J., Schröter, C., & Hadjantonakis, A.-K. (2018) · Developmental Biology · doi:10.1016/j.ydbio.2018.06.017 · Cited by 55
Weng, Z., Xu, C., Chen, X., Yan, Q., Fu, Z., Jiao, J., Xu, J., Liu, Q., Wang, D., Liang, J., et al. (2024) · Environment International · doi:10.1016/j.envint.2024.108477 · Cited by 5
Metadata
- Authors
- Su, N., Jin, M., & Chen, L.
- Venue
- Bone Research
- Published
- 2014-04-29
- Volume
- 2
- Issue
- 1
- Pages
- 14003-14003
- ISSN
- 2095-4700 (ISSN-L)
- 2095-6231
- OpenAlex
- W2004632928
- Cited by
- 290
- References
- 251
- FWCI
- 6.45
- Type
- journal article
- Language
- en
- Open access
- gold
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
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Role of FGF/FGFR signaling in skeletal development and homeostasis: learning from mouse models. https://app.cochat.ai/papers/10.1038/boneres.2014.3
- The paper
- Su, N., Jin, M., & Chen, L. (2014). Role of FGF/FGFR signaling in skeletal development and homeostasis: learning from mouse models. Bone Research. https://doi.org/10.1038/boneres.2014.3
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.
