Future science OA · 2025
TWEAK/Fn14 axis may promote vascular smooth muscle cell senescence via p38 signaling pathway: preliminary evidence.
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Wei Chunyang, Liu Xiaoying, Miao Zhuang, Zhang Hua, Wang Yanfu, Qi Guoxian
Аннотация
AIM: The primary objective of this study is to investigate the impact of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its functional receptor, fibroblast growth factor-inducible 14 (Fn14), on the process of vascular smooth muscle cell (VSMC) senescence.
METHODS: Rat arterial VSMCs were cultured with angiotensin II to establish a model of premature senescence. The effects of TWEAK and Fn14 on senescent VSMCs were evaluated. Additionally, the role of p38 phosphorylation pathway in the effect of TWEAK on VSMCs senescence was assessed.
RESULTS: Expressions of TWEAK and Fn14 were significantly elevated in senescent VSMCs. TWEAK activated the p38 phosphorylation pathway and promoted the SA-β-gal staining and P53 expression.
CONCLUSION: These preliminary findings suggest that the TWEAK/Fn14 axis may play a crucial role in promoting VSMC senescence.
METHODS: Rat arterial VSMCs were cultured with angiotensin II to establish a model of premature senescence. The effects of TWEAK and Fn14 on senescent VSMCs were evaluated. Additionally, the role of p38 phosphorylation pathway in the effect of TWEAK on VSMCs senescence was assessed.
RESULTS: Expressions of TWEAK and Fn14 were significantly elevated in senescent VSMCs. TWEAK activated the p38 phosphorylation pathway and promoted the SA-β-gal staining and P53 expression.
CONCLUSION: These preliminary findings suggest that the TWEAK/Fn14 axis may play a crucial role in promoting VSMC senescence.