Role of RANK ligand in mediating increased bone resorption in early postmenopausal women.
By G. Eghbali-Fatourechi, S. Khosla, A. Sanyal, W. J. Boyle, D. Lacey, B. Riggs. Journal of Clinical Investigation, 2003
804 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology, Orthopedics and Sports Medicine
View Paper: https://www.semanticscholar.org/paper/396319b3fc92555280716e7625edd7f7c511ea03
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Citations in the corpus
- Effects of obesity on bone metabolism (2011, neutral): “RANKL [39,43,44].”
- Estrogen and the Skeleton (2012, positive): “Combined in vitro and in vivo studies have demonstrated that estrogen suppresses RANKL production by osteoblastic, T- and B-cells (34) and also increases production of the decoy receptor for RANKL, osteoprotegerin (OPG) (35, 36).”
- Denosumab and bisphosphonates: different mechanisms of action and effects. (2011, background): “Increased expression and production of RANK ligand (RANKL), as seen with estrogen deprivation, is a central mechanism of osteoclast activation and increased bone resorption [8,9].”
- Genetic regulation of osteoclast development and function (2003, background): “A recent seminal report shows that women who lack oestrogen have higher expression of the important osteoclastogenic molecule RANKL on both osteoblasts and lymphocyte”
- Receptor activator of nuclear factor kappaB ligand and osteoprotegerin regulation of bone remodeling in health and disease. (2008, neutral): “and inversely with serum estradiol levels (76).”