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|Title:||TWEAK and TNF regulation of sclerostin: a novel pathway for the regulation of bone remodelling|
|Citation:||Advances in TNF Family Research, 2011 / Wallach, D., Kovalenko, A., Feldmann, M. (ed./s), pp.337-348|
|Publisher Place:||233 Spring St New York NY 10013|
|Series/Report no.:||Advances in Experimental Medicine and Biology ; 691|
|David M. Findlay and Gerald J. Atkins|
|Abstract:||Bone remodelling is the critical process, by which skeletal mass and integrity are controlled. This process is disrupted in a number of bone pathologies, such as osteoporosis, and the focal bone loss that occurs in rheumatoid arthritis, around artificial joint prostheses or that induced by osteolytic tumours. A common feature of conditions that result in a net loss of bone is the presence of elevated levels of pro-inflammatory mediators and evidence has accumulated to show that a chronic inflammatory environment is both catabolic for bone and may also suppress bone formation. Here, we focus on the possible anti-anabolic roles in bone of TNFα and TNF-like weak inducer of apoptosis (TWEAK).|
|Keywords:||Osteoblasts; Humans; Tumor Necrosis Factors; Bone Morphogenetic Proteins; Receptors, Tumor Necrosis Factor; Bone Remodeling; Signal Transduction; Transcription, Genetic; Calcification, Physiologic; Protein Binding; Osteogenesis; Models, Biological; Wnt Proteins|
|Rights:||© Springer Science+Business Media, LLC 2011|
|Appears in Collections:||Orthopaedics and Trauma publications|
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