NF-κB signaling and bone resorption
Identifieur interne : 005677 ( Ncbi/Merge ); précédent : 005676; suivant : 005678NF-κB signaling and bone resorption
Auteurs : Y. Abu-AmerSource :
- Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA [ 0937-941X ] ; 2013.
Abstract
The transcription factor NF-κB is a family of proteins involved in signaling pathways essential for normal cellular functions and development. Deletion of various components of this pathway resulted with abnormal skeletal development. Research in the last decade has established that NF-κB signaling mediates RANK ligand-induced osteoclastogenesis. Consistently, it was shown that inhibition of NF-κB was an effective approach to inhibit osteoclast formation and bone resorptive activity. Identification of the molecular machinery underlying NF-κB activation permitted osteoclast-specific deletion of the major components of this pathway. As a result, it was clear that deletion of members of the proximal IKK kinase complex and the distal NF-κB subunits and downstream regulators affected skeletal development. These studies provided several targets of therapeutic intervention in osteolytic diseases. NF-κB activity has been also described as the centerpiece of inflammatory responses and is considered a potent mediator of inflammatory osteolysis. Indeed, inflammatory insults exacerbate physiologic RANKL-induced NF-κB signals leading to exaggerated responses and to inflammatory osteolysis. These superimposed NF-κB activities appear to underlie several bone pathologies. This review will describe the individual roles of NF-κB molecules in bone resorption and inflammatory osteolysis.
Url:
DOI: 10.1007/s00198-013-2313-x
PubMed: 23468073
PubMed Central: 3884829
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PMC:3884829Le document en format XML
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<front><div type="abstract" xml:lang="en"><p id="P1">The transcription factor NF-κB is a family of proteins involved in signaling pathways essential for normal cellular functions and development. Deletion of various components of this pathway resulted with abnormal skeletal development. Research in the last decade has established that NF-κB signaling mediates RANK ligand-induced osteoclastogenesis. Consistently, it was shown that inhibition of NF-κB was an effective approach to inhibit osteoclast formation and bone resorptive activity. Identification of the molecular machinery underlying NF-κB activation permitted osteoclast-specific deletion of the major components of this pathway. As a result, it was clear that deletion of members of the proximal IKK kinase complex and the distal NF-κB subunits and downstream regulators affected skeletal development. These studies provided several targets of therapeutic intervention in osteolytic diseases. NF-κB activity has been also described as the centerpiece of inflammatory responses and is considered a potent mediator of inflammatory osteolysis. Indeed, inflammatory insults exacerbate physiologic RANKL-induced NF-κB signals leading to exaggerated responses and to inflammatory osteolysis. These superimposed NF-κB activities appear to underlie several bone pathologies. This review will describe the individual roles of NF-κB molecules in bone resorption and inflammatory osteolysis.</p>
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<contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Abu-Amer</surname>
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<aff id="A1">Department of Orthopedic Surgery, Department of Cell Biology & Physiology, Washington University School of Medicine, 660S. Euclid Avenue, Saint Louis, MO 63110, USA,<email>abuamery@wustl.edu</email>
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<pub-date pub-type="pmc-release"><day>08</day>
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<volume>24</volume>
<issue>9</issue>
<elocation-id>10.1007/s00198-013-2313-x</elocation-id>
<permissions><copyright-statement>© International Osteoporosis Foundation and National Osteoporosis Foundation 2013</copyright-statement>
<copyright-year>2013</copyright-year>
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<abstract><p id="P1">The transcription factor NF-κB is a family of proteins involved in signaling pathways essential for normal cellular functions and development. Deletion of various components of this pathway resulted with abnormal skeletal development. Research in the last decade has established that NF-κB signaling mediates RANK ligand-induced osteoclastogenesis. Consistently, it was shown that inhibition of NF-κB was an effective approach to inhibit osteoclast formation and bone resorptive activity. Identification of the molecular machinery underlying NF-κB activation permitted osteoclast-specific deletion of the major components of this pathway. As a result, it was clear that deletion of members of the proximal IKK kinase complex and the distal NF-κB subunits and downstream regulators affected skeletal development. These studies provided several targets of therapeutic intervention in osteolytic diseases. NF-κB activity has been also described as the centerpiece of inflammatory responses and is considered a potent mediator of inflammatory osteolysis. Indeed, inflammatory insults exacerbate physiologic RANKL-induced NF-κB signals leading to exaggerated responses and to inflammatory osteolysis. These superimposed NF-κB activities appear to underlie several bone pathologies. This review will describe the individual roles of NF-κB molecules in bone resorption and inflammatory osteolysis.</p>
</abstract>
<kwd-group><kwd>IKK</kwd>
<kwd>NF-κB</kwd>
<kwd>Osteoclast</kwd>
<kwd>Osteolysis</kwd>
</kwd-group>
<funding-group><award-group><funding-source country="United States">National Institute of Arthritis and Musculoskeletal and Skin Diseases : NIAMS</funding-source>
<award-id>R01 AR054326 || AR</award-id>
</award-group>
<award-group><funding-source country="United States">National Institute of Arthritis and Musculoskeletal and Skin Diseases : NIAMS</funding-source>
<award-id>R01 AR049192 || AR</award-id>
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