The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Clinical Implications of the Osteoprotegerin/RANKL/RANK System for Bone and Vascular Diseases
Abstract
Bone resorption by osteoclasts is coupled with bone formation by osteoblasts, and this balanced process continuously remodels and adapts the skeleton. The receptor activator of nuclear factor kappaB ligand (RANKL) has been identified as an essential cytokine for the formation and activation of osteoclasts. The effects of RANKL are physiologically counterbalanced by the decoy receptor osteoprotegerin (OPG). Estrogen deficiency, glucocorticoid exposure, T-cell activation (eg, rheumatoid arthritis), and skeletal malignancies (eg, myeloma, metastases) enhance the ratio of RANKL to OPG and, thus, promote osteoclastogenesis, accelerate bone resorption, and induce bone loss. Moreover, alterations of the OPG/RANKL/RANK system have been implicated in vascular diseases. RANKL blockade (using OPG or RANK fusion proteins or RANKL antibodies) has prevented bone loss caused by osteoporosis, chronic inflammatory disorders, and malignant tumors in animal models and may emerge as a therapy in humans based on studies in postmenopausal osteoporosis, myeloma bone disease, and osteolytic metastases. This review summarizes the clinical implications of the OPG/RANKL/RANK system for bone and vascular diseases.
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Cites
Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation.
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Osteoprotegerin: a novel secreted protein involved in the regulation of bone density.
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Bone Resorption by Osteoclasts
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Role of RANK ligand in mediating increased bone resorption in early postmenopausal women
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Breast Cancer Cells Interact with Osteoblasts to Support Osteoclast Formation1
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Cited by
Functions 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
Inflammatory and immune pathways in the pathogenesis of periodontal disease
Cekici, A., Kantarci, A., Hasturk, H., & Van Dyke, T. E. (2014) · Periodontology 2000 · doi:10.1111/prd.12002 · Cited by 1,415
“osteoporosis, cancer-related bone metastasis and diabetes-associated alveolar bone destruction (25, 87, 89, 122, 158, 169), confirming the critical role of the RANKL ⁄ RANK ⁄ osteoprotegerin triad in osteoclas-”
BackgroundBone, H. G., Wagman, R. B., Brandi, M. L., Brown, J. P., Chapurlat, R., Cummings, S. R., Czerwiński, E., Fahrleitner-Pammer, A., Kendler, D. L., Lippuner, K., et al. (2017) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(17)30138-9 · Cited by 996
Biology of RANK, RANKL, and osteoprotegerin
Boyce, B. F., & Xing, L. (2007) · Arthritis Research & Therapy · doi:10.1186/ar2165 · Cited by 957
Understanding multiple myeloma pathogenesis in the bone marrow to identify new therapeutic targets
Hideshima, T., Mitsiades, C., Tonon, G., Richardson, P. G., & Anderson, K. C. (2007) · Nature Reviews Cancer · doi:10.1038/nrc2189 · Cited by 932
Metadata
- Authors
- Hofbauer, L. C.
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 2004-07-28
- Volume
- 292
- Issue
- 4
- Pages
- 490
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- OpenAlex
- W2128843508
- Cited by
- 988
- References
- 45
- FWCI
- 17.49
- Type
- journal article
- Language
- en
- Open access
- closed
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