Targeting the JNK-JUN-NCOA4 Axis to Treat Macrophage Ferroptosis in Chronic Apical Periodontitis
Author Information
Author(s): Wang Yuting, Li Wenlan, Mu Wenli, Seyam Abdelrahman, Guan Yonghui, Tang Yifei, Wang Mingfei, Xin Ying, Guo Xiaomei, Hou Tiezhou, Guan Xiaoyue
Primary Institution: Xi'an Jiaotong University, Xi'an, Shaanxi, China
Hypothesis
This study aimed to investigate the involvement of macrophage ferroptosis in chronic apical periodontitis (CAP) and determine if blocking the JNK/JUN/NCOA4 axis could alleviate CAP by regulating macrophage ferroptosis.
Conclusion
Targeting the JNK/JUN/NCOA4 axis is an effective therapeutic strategy to rescue periapical lesions from inflammation due to its anti-macrophage ferroptosis function.
Supporting Evidence
- The in vitro AP model demonstrated that macrophage ferroptosis mainly occurred during the late phase of inflammatory conditions.
- A higher accumulation of iron was observed in the periapical lesions derived from clinical samples and animal models.
- The inhibition of the JNK/JUN/NCOA4 axis reduced changes and inflammation levels induced by E. coli LPS in macrophages.
- Macrophage ferroptosis contributes to the development of CAP.
- Targeting the JNK/JUN/NCOA4 axis provides support for further investigation as a targeted signaling pathway for CAP treatment.
Takeaway
This study found that a type of cell death called ferroptosis in immune cells can make a dental condition worse, but blocking a specific pathway in these cells can help treat the problem.
Methodology
The study used in vitro models of apical periodontitis and in vivo models including clinical specimens and rats' periapical lesions to investigate macrophage ferroptosis and the JNK/JUN/NCOA4 axis.
Participant Demographics
Participants were aged 22-50, free of systemic diseases, and had not used antibiotics in the previous 6 months.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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