Oral diseases · 2025
DDX5 Alleviates Temporomandibular Joint Osteoarthritis via TNF-Induced NF-κB Signaling Pathway.
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Liang Qingqing, Han Peiru, Han Mingrui, Wang Mengjia, Zhao Qing, Zhang Yuan, Ye Chuanjin, Chen Sheng, Fang Bing, Sun Yang, Ji Jun
Аннотация
BACKGROUND: Temporomandibular joint osteoarthritis (TMJOA) is a prevalent musculoskeletal condition characterized by pain, cartilage degeneration, and subchondral bone loss.
OBJECTIVE: This study sought to identify specific targets for the treatment of TMJOA.
METHOD: Through high-throughput RNA-seq analysis in condylar chondrocytes (NC vs. MS), we discovered that DDX5 was downregulated and closely negatively related to the progression of TMJOA. Similarly, we found that DDX5 was downregulated in injured condylar cartilage of patients as well as the condyles of UAC-induced TMJOA mice. The chondrocyte-specific deletion of Ddx5 aggravated tissue destruction in TMJOA modeling by inducing degradation of extracellular matrix (ECM).
RESULTS: The loss of DDX5 facilitated chondrocyte degradation and the occurrence of joint inflammation in condylar chondrocytes. In addition, the local injection of AAV overexpressing DDX5 significantly alleviated inflammation, cartilage degradation, and subchondral bone loss in TMJOA mice. RNA-seq analysis revealed that the DDX5 deficiency mostly activated the TNF-induced nuclear factor-kappa B (NF-κB) signaling pathway causing the occurrence of TMJOA.
CONCLUSION: Mechanistically, the inhibition of DDX5 accelerated cartilage degeneration by activating TNF-induced NF-κB signaling. Thus, DDX5 emerges as a potential effective drug target for future therapeutic approaches in TMJOA.
OBJECTIVE: This study sought to identify specific targets for the treatment of TMJOA.
METHOD: Through high-throughput RNA-seq analysis in condylar chondrocytes (NC vs. MS), we discovered that DDX5 was downregulated and closely negatively related to the progression of TMJOA. Similarly, we found that DDX5 was downregulated in injured condylar cartilage of patients as well as the condyles of UAC-induced TMJOA mice. The chondrocyte-specific deletion of Ddx5 aggravated tissue destruction in TMJOA modeling by inducing degradation of extracellular matrix (ECM).
RESULTS: The loss of DDX5 facilitated chondrocyte degradation and the occurrence of joint inflammation in condylar chondrocytes. In addition, the local injection of AAV overexpressing DDX5 significantly alleviated inflammation, cartilage degradation, and subchondral bone loss in TMJOA mice. RNA-seq analysis revealed that the DDX5 deficiency mostly activated the TNF-induced nuclear factor-kappa B (NF-κB) signaling pathway causing the occurrence of TMJOA.
CONCLUSION: Mechanistically, the inhibition of DDX5 accelerated cartilage degeneration by activating TNF-induced NF-κB signaling. Thus, DDX5 emerges as a potential effective drug target for future therapeutic approaches in TMJOA.