Clinical implications of the osteoprotegerin/RANKL/RANK system for bone and vascular diseases.
By L. Hofbauer, M. Schoppet. Journal of the American Medical Association (JAMA), 2004
1,014 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology, Orthopedics and Sports Medicine
View Paper: https://www.semanticscholar.org/paper/300b17bba11ee7b633492c05e23a4e351af25513
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Citations in the corpus
- Inflammatory and immune pathways in the pathogenesis of periodontal disease (2014, background): “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-”
- Biology of RANK, RANKL, and osteoprotegerin (2007, background): “Many reports have supported the assertion that the RANKL/OPG ratio is a major determinant of bone mass [28].”
- Understanding multiple myeloma pathogenesis in the bone marrow to identify new therapeutic targets (2007, background): “RANKL binds to RANK on osteoclasts, thereby stimulating their differentiation and activity, whereas OPG functions as a decoy receptor by binding to RANKL and preventing its interaction with RANK, thereby inhibiting its ability to stimulate osteoclastogenesi”