Shenzhen Key Laboratory for Anti-ageing and Regenerative Medicine, Guangdong Key Laboratory for Genome Stability and Disease Prevention, Department of Medical Cell Biology and Genetics, Shenzhen University Health Science Center, Shenzhen 518060, China.
National Pharmaceutical Engineering Center for Solid Preparation in Chinese Herbal Medicine, Jiangxi University of Traditional Chinese Medicine, Nanchang 330006, China.
Int J Mol Sci. 2018 Nov 28;19(12):3794. doi: 10.3390/ijms19123794.
Chondrocyte dysfunction occurs during the development of osteoarthritis (OA), typically resulting from a deleterious increase in oxidative stress. Accordingly, strategies for arresting oxidative stress-induced chondrocyte dysfunction may lead to new potential therapeutic targets for OA treatment. Forkhead box O (FoxO) transcription factors have recently been shown to play a protective role in chondrocyte dysfunction through the regulation of inflammation, autophagy, aging, and oxidative stress. They also regulate growth, maturation, and matrix synthesis in chondrocytes. In this review, we discuss the recent progress made in the field of oxidative stress-induced chondrocyte dysfunction. We also discuss the protective role of FoxO transcription factors as potential molecular targets for the treatment of OA. Understanding the function of FoxO transcription factors in the OA pathology may provide new insights that will facilitate the development of next-generation therapies to prevent OA development and to slow OA progression.
软骨细胞功能障碍发生在骨关节炎 (OA) 的发展过程中，通常是由于氧化应激的有害增加所致。因此，阻止氧化应激诱导的软骨细胞功能障碍的策略可能为 OA 治疗提供新的潜在治疗靶点。叉头框 O (FoxO) 转录因子最近被证明通过调节炎症、自噬、衰老和氧化应激在软骨细胞功能障碍中发挥保护作用。它们还调节软骨细胞的生长、成熟和基质合成。在这篇综述中，我们讨论了氧化应激诱导的软骨细胞功能障碍领域的最新进展。我们还讨论了 FoxO 转录因子作为 OA 治疗的潜在分子靶点的保护作用。了解 FoxO 转录因子在 OA 病理中的功能可能提供新的见解，有助于开发下一代疗法来预防 OA 的发展和减缓 OA 的进展。
