NF-κB Signaling Pathways in Osteoarthritic Cartilage Destruction

Cells. 2019 Jul 17;8(7):734. doi: 10.3390/cells8070734.

Abstract

Osteoarthritis (OA) is a type of joint disease associated with wear and tear, inflammation, and aging. Mechanical stress along with synovial inflammation promotes the degradation of the extracellular matrix in the cartilage, leading to the breakdown of joint cartilage. The nuclear factor-kappaB (NF-κB) transcription factor has long been recognized as a disease-contributing factor and, thus, has become a therapeutic target for OA. Because NF-κB is a versatile and multi-functional transcription factor involved in various biological processes, a comprehensive understanding of the functions or regulation of NF-κB in the OA pathology will aid in the development of targeted therapeutic strategies to protect the cartilage from OA damage and reduce the risk of potential side-effects. In this review, we discuss the roles of NF-κB in OA chondrocytes and related signaling pathways, including recent findings, to better understand pathological cartilage remodeling and provide potential therapeutic targets that can interfere with NF-κB signaling for OA treatment.

Keywords: IκBζ; cartilage degeneration; chondrocyte apoptosis; chondrocyte catabolism; osteoarthritis; NF-κB.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Cartilage / metabolism*
  • Cartilage / pathology
  • Epigenesis, Genetic
  • Humans
  • NF-kappa B / genetics
  • NF-kappa B / metabolism*
  • Osteoarthritis / genetics
  • Osteoarthritis / metabolism*
  • Osteoarthritis / pathology
  • Signal Transduction

Substances

  • NF-kappa B