Department of Biomedical Science, Chosun University, Gwangju 61452, Korea.
Department of Bioinformatics, Kongju National University, Kongju 38065, Korea.
Cells. 2019 Jul 17;8(7):734. doi: 10.3390/cells8070734.
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.
骨关节炎（OA）是一种与磨损、炎症和衰老有关的关节疾病。机械应力和滑膜炎症促进软骨细胞外基质的降解，导致关节软骨的破坏。核因子-κB（NF-κB）转录因子一直被认为是一种致病因素，因此已成为 OA 的治疗靶点。由于 NF-κB 是一种多功能转录因子，参与多种生物学过程，因此全面了解 NF-κB 在 OA 病理中的功能或调节将有助于开发靶向治疗策略，以保护软骨免受 OA 损伤并降低潜在副作用的风险。在这篇综述中，我们讨论了 NF-κB 在 OA 软骨细胞中的作用及其相关信号通路，包括最近的发现，以更好地理解病理性软骨重塑，并提供潜在的治疗靶点，以干扰 NF-κB 信号通路用于 OA 的治疗。
