The Role of BMP Signaling and NF-κB Signaling on Osteoblastic Differentiation, Cancer Development, and Vascular Diseases-Is the Activation of NF-κB a Friend or Foe of BMP Function?

Research output: Chapter in Book/Report/Conference proceedingConference contribution

3 Citations (Scopus)

Abstract

Bone morphogenetic proteins (BMPs), members of the transforming growth factor-β family, were first identified as potent inducers of ectopic bone formation when implanted into muscle tissue. Subsequent studies have demonstrated that BMPs play important roles during developmental processes, including cell proliferation, differentiation, and apoptosis. Furthermore, recent studies have shown that BMPs are also involved in the initiation and/or progression of various diseases, such as skeletal diseases, cancer, and vascular diseases. Nuclear factor κ light-chain enhancer of activated B cells (NF-κB) was originally identified as a transcription factor that bound to the enhancer region of the immunoglobulin κ light-chain promoter in B cells. A wide range of stimuli, including inflammatory cytokines and bacterial and viral products, activate the NF-κB pathway, leading to the expression of NF-κB target genes. NF-κB also has functions in multiple biological processes, such as immune and inflammatory responses, cell differentiation, cellular stress responses, and cancer development. Recent findings have demonstrated that BMP and NF-κB signaling agonistically or antagonistically regulate bone development, cancer development, and vascular diseases. This review describes the role of BMPs and NF-κB in bone development, cancer development, and vascular diseases with special attention given to concepts that have emerged in recent years.

Original languageEnglish
Title of host publicationBone Morphogenic Protein, 2015
EditorsGerald Litwack
PublisherAcademic Press Inc.
Pages145-170
Number of pages26
ISBN (Print)9780128024423
DOIs
Publication statusPublished - Jan 1 2015
Externally publishedYes

Publication series

NameVitamins and Hormones
Volume99
ISSN (Print)0083-6729

All Science Journal Classification (ASJC) codes

  • Physiology
  • Endocrinology

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