Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 19, Issue 12, Pages -Publisher
MDPI
DOI: 10.3390/ijms19123794
Keywords
chondrocyte dysfunction; osteoarthritis; FoxO; oxidative stress; autophagy; aging; articular cartilage; molecular target
Funding
- National Natural Science Foundation of China [81560662, 81803536, 81472126]
- China Postdoctoral Science Foundation [2017M610543]
- Shenzhen Basic Research Projects [JCYJ20170818100811018, JCYJ20160226192924528, GGFW2016030117123665, JCYJ20160331114205502]
- Shenzhen Development and Reform Committee for Shenzhen Engineering Laboratory of Orthopedic Regenerative Technologies
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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.
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