The NF-κB signalling pathway in osteoarthritis

•Osteoarthritis (OA) is a degenerative disease affecting all compartments of the joint.•NF-κB signalling pathway is a major catabolic pathway in OA joints.•NF-κB triggers the expression of various genes which are implicated in cartilage destruction, synovial membrane inflammation and increased subch...

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Bibliographic Details
Published inThe international journal of biochemistry & cell biology Vol. 45; no. 11; pp. 2580 - 2584
Main Authors Rigoglou, Stella, Papavassiliou, Athanasios G.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Ltd 01.11.2013
Subjects
Animals
Arrays
Biocompatibility
Biomedical materials
Cartilage destruction
chemokines
Chondrocytes
Cytokines
Degradation
evolution
extracellular matrix
Gene expression
genes
Humans
Models, Biological
NF-kappa B - metabolism
NF-κB
Osteoarthritis
Osteoarthritis - metabolism
Osteoarthritis - pathology
Osteoarthritis - therapy
pathogenesis
Pathways
proteins
Signal Transduction
Signalling
transcription factor NF-kappa B
NF-κB
Signal transduction
Cartilage destruction
Osteoarthritis
Chondrocytes
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Summary:•Osteoarthritis (OA) is a degenerative disease affecting all compartments of the joint.•NF-κB signalling pathway is a major catabolic pathway in OA joints.•NF-κB triggers the expression of various genes which are implicated in cartilage destruction, synovial membrane inflammation and increased subchondral bone resorption.•Targeting of the NF-κB signalling cascade is a promising therapeutic strategy for OA treatment. Nuclear factor-kappaB (NF-κB) proteins constitute a family of transcription factors that are stimulated by pro-inflammatory cytokines, chemokines, stress-related factors and extracellular matrix (ECM) degradation products. Upon stimulation, the activated NF-κB molecules trigger the expression of an array of genes which induce destruction of the articular joint, leading to osteoarthritis (OA) onset and progression. Therefore, targeted strategies that interfere with NF-κB signalling could offer novel potential therapeutic options for OA treatment. In this review, we discuss the involvement of NF-κB in OA pathogenesis and how pharmacological inhibition of the NF-κB signalling pathway affects OA incidence and evolution.
Bibliography:http://dx.doi.org/10.1016/j.biocel.2013.08.018
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ISSN:1357-2725
1878-5875
1878-5875
DOI:10.1016/j.biocel.2013.08.018