Evidence for osteocyte regulation of bone homeostasis through RANKL expression

By T. Nakashima, M. Hayashi, T. Fukunaga, K. Kurata, M. Oh‐hora, Jian Q. Feng, L. Bonewald, T. Kodama, Anton Wutz, E. Wagner and 2 more. Nature Medicine, 2011

1,711 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Orthopedics and Sports Medicine

View Paper: https://www.semanticscholar.org/paper/fe4e3ae2c382a28af2f6697d678ee9a6a7da4e1c

How researchers see this paper

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In Molecular Biology

1. J. H. Park
2. R. Florêncio-Silva
3. E. Sasso-Cerri
4. M. Simões
5. S. Khosla
6. G. R. S. Sasso
7. Soo Young Lee
8. P. Cerri

In Oncology

1. J. H. Park
2. S. Khosla
3. Soo Young Lee
4. T. Martin
5. N. Lee
6. N. Sims
7. D. Monroe
8. M. Oursler

In Orthopedics and Sports Medicine

1. S. Khosla
2. D. Monroe
3. M. Oursler
4. M. F. Holick

Citations in the corpus

• Current Understanding of RANK Signaling in Osteoclast Differentiation and Maturation (2017, background): “, 2014) or osteocytes (Nakashima et al., 2011; Xiong et al., 2011), are required for the differentiation of osteoclast precursors into mature osteoclasts (Teitelbaum and Ross, 2003).”
• Coupling the activities of bone formation and resorption: a multitude of signals within the basic multicellular unit. (2014, result): “Notable in the latter work, in direct contrast to the findings of Nakashima et al.(36), was that RANKL mRNA levels were higher in osteoblastrich cell preparations compared with osteocyte-rich preparations.”
• Estrogen and the Skeleton (2012, positive): “Moreover, given the recent evidence noted above for the osteocyte being an important source of RANKL in bone (12, 13), it is possible that osteocyte apoptosis results in an increase in RANKL in the bone microenvironment, perhaps due to RANKL release from the apoptotic osteocytes or via effects of th”
• Atypical Subtrochanteric and Diaphyseal Femoral Fractures: Second Report of a Task Force of the American Society for Bone and Mineral Research (2011, background): “Stress fractures heal by targeted remodeling of the injured site through a process of osteocyte apoptosis, which signals for repair through elevated production of receptor activator of NF‐kB ligand (RANKL),((71,72)) osteoclastic resorption to remove the damage, and then osteoblastic formation to rep”
• Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells (2015, background): “There is evidence that osteocytes act as the main source of RANKL to promote osteoclastogenesis [167, 168], although this factor has also been demonstrated to be produced by other cell types such as stromal cells [194], osteoblasts, and fibroblasts [88, 89].”