TWEAK/Fn14轴可能通过p38信号通路促进血管光滑肌肉细胞衰老:初步证据
Chunyang Wei1, Xiaoying Liu1, Zhuang Miao2
1Department of Gerontology, the First Affiliated Hospital, Dalian Medical University, Dalian, China.
Future science OA
|January 22, 2025
概括
TWEAK/Fn14通路促进了血管光滑肌细胞 (VSMC) 的衰老. 这个轴激活了p38通路,增加了VSMC中的SA-β-gal和P53表达等衰老标志物.
科学领域:
- 心血管生物学 心血管生物学
- 细胞衰老 细胞衰老
- 分子信号传输的方法
背景情况:
- 血管光滑肌细胞 (VSMC) 衰老有助于心血管疾病.
- 特定分子通路在VSMC衰老中的作用需要进一步阐明.
研究的目的:
- 为了研究瘤亡因子类弱诱导亡因子 (TWEAK) 和其受体纤维细胞生长因子诱导14 (Fn14) 对VSMC衰老的影响.
- 评估p38酸化途径在TWEAK诱导的VSMC衰老中的参与.
主要方法:
- 建立了一个大鼠动脉VSMC衰老模型,使用血管激素II.
- 评估了TWEAK和Fn14对老化的VSMC的影响.
- 评估了p38酸化通路的激活.
主要成果:
- 在老化的VSMC中,TWEAK和Fn14表达显著增加.
- TWEAK激活了p38酸化途径.
- TWEAK促进了SA-β-gal染色和P53表达,表明衰老的增加.
结论:
- TWEAK/Fn14轴在促进VSMC衰老方面发挥着重要作用.
- p38酸化途径参与TWEAK介导的VSMC衰老.
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