Oral diseases · 2026
IL-17A Induces Chondrocyte Senescence via the STAT3-OPA1-mtROS Axis in Temporomandibular Joint Osteoarthritis.
СтатьяНазвание и аннотация: Перевод в очереди
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Zhu Mengqi, Zhang Chunyan, Zhang Yangyang, Zhang Congdi, Wu Zuping, Wang Ying, Qu Linghan, Wu Mengjie, Shen Minjuan, Chen Qianming, Shi Jiejun
Аннотация
OBJECTIVES: To elucidate the pathogenic mechanisms underlying interleukin-17A (IL-17A) induced chondrocyte senescence in TMJ-OA and provide preclinical evidence supporting IL-17A as a novel therapeutic target for TMJ-OA.
METHODS: We established a TMJ-OA mouse model using unilateral anterior crossbite (UAC) to investigate IL-17A expression and chondrocyte senescence. We subsequently cultured ATDC5 mouse chondrocytes with IL-17A in vitro to assess cellular senescence and further explored mitochondrial-related mechanisms. Finally, we evaluated the inhibitory effect of Secukinumab (an anti-IL-17A monoclonal antibody) on chondrocyte senescence and pathological progression in TMJ-OA mice.
RESULTS: Chondrocyte senescence is positively correlated with the expression of IL-17A in the condylar cartilage of TMJ-OA mice. IL-17A can induce cellular senescence in ATDC5 cells in vitro. Mechanistically, IL-17A increased the expression of the mitochondrial fusion-related protein optic atrophy 1 (OPA1) by increasing the phosphorylation level of signal transducer and activator of transcription 3 (STAT3). This caused mitochondrial hyperfusion and an increase in mitochondrial reactive oxygen species (mtROS), contributing to mitochondrial dysfunction and cellular senescence. Moreover, Secukinumab reduced chondrocyte senescence and inhibited pathological progression in TMJ-OA mice.
CONCLUSION: IL-17A induces chondrocyte senescence by promoting mitochondrial dysfunction through a STAT3-OPA1-mtROS-dependent axis, and IL-17A may serve as a therapeutic target for the treatment of TMJ-OA.
METHODS: We established a TMJ-OA mouse model using unilateral anterior crossbite (UAC) to investigate IL-17A expression and chondrocyte senescence. We subsequently cultured ATDC5 mouse chondrocytes with IL-17A in vitro to assess cellular senescence and further explored mitochondrial-related mechanisms. Finally, we evaluated the inhibitory effect of Secukinumab (an anti-IL-17A monoclonal antibody) on chondrocyte senescence and pathological progression in TMJ-OA mice.
RESULTS: Chondrocyte senescence is positively correlated with the expression of IL-17A in the condylar cartilage of TMJ-OA mice. IL-17A can induce cellular senescence in ATDC5 cells in vitro. Mechanistically, IL-17A increased the expression of the mitochondrial fusion-related protein optic atrophy 1 (OPA1) by increasing the phosphorylation level of signal transducer and activator of transcription 3 (STAT3). This caused mitochondrial hyperfusion and an increase in mitochondrial reactive oxygen species (mtROS), contributing to mitochondrial dysfunction and cellular senescence. Moreover, Secukinumab reduced chondrocyte senescence and inhibited pathological progression in TMJ-OA mice.
CONCLUSION: IL-17A induces chondrocyte senescence by promoting mitochondrial dysfunction through a STAT3-OPA1-mtROS-dependent axis, and IL-17A may serve as a therapeutic target for the treatment of TMJ-OA.