在慢性病中,ZBTB16通过加速的VSMCS驱动血管化,通过WNT/Β-CATENIN PATHWAY通过慢性病驱动血管化
Yan Shen, Huaxing Huang1, Lianglan Shen1
1Department of Nephrology, The Second Affiliated Hospital of Nantong University, Nantong, China.
Shock (Augusta, Ga.)
|October 25, 2024
概括
含有16 (ZBTB16) 的指和BTB域促进慢性病 (CKD) 的血管化. 沉默ZBTB16通过Wnt/β-catenin通路抑制VSMC骨质细胞转化,从而减少化和功能障碍.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 血管生物学 血管生物学
- 分子生物学分子生物学
背景情况:
- 血管化 (VC) 是慢性病 (CKD) 的常见并发症,由血管光滑肌细胞 (VSMC) 现型转变驱动.
- 在VC模型中注意到指和BTB域含有16 (ZBTB16) 表达式,这表明一个潜在的角色.
研究的目的:
- 研究ZBTB16在CKD相关的VC中的功能.
- 阐明VC中ZBTB16的潜在分子机制.
主要方法:
- 建立了体内CKD老鼠模型和体内高酸盐刺激的VSMC化模型.
- 评估功能,动脉化和VSMC骨质细胞分化.
- 使用分子生物学技术量化ZBTB16表达和Wnt/β-catenin通路信号蛋白.
主要成果:
- 在CKD患者中,ZBTB16表达显著升高,CKD患者有VC,CKD老鼠大动脉和高酸盐处理的VSMC.
- 镇压ZBTB16改善了功能障碍,减少了沉积,并在体外和体内抑制了VSMC骨质细胞分化.
- 沉默ZBTB16使Wnt/β-catenin通路失活,而Wnt/β-catenin激动剂LiCl逆转了ZBTB16敲击的保护作用.
结论:
- ZBTB16在促进CKD相关的VC中发挥着至关重要的作用.
- 通过降低Wnt/β-catenin通路的调节,ZBTB16沉默通过抑制VSMC骨质细胞转化来保护VC.
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