USP18通过抑制JAK/STAT通路来抑制代谢性高血压的进展
Zhihong Xie1, Mingshan Huang2, Wang Xu2
1Department of Cardiology, Ganzhou People's Hospital, 16 Meiguan Dadao, Zhanggong District, Ganzhou, 341000, Jiangxi, China. xzh8880@163.com.
Cardiovascular toxicology
|May 1, 2024
概括
乌比基特异性蛋白酶18 (USP18) 通过增强细胞增殖,逆转细胞亡和氧化应激,并抑制JAK/STAT通路来抑制代谢性高血压的进展. 这一发现为代谢性高血压 (MHR) 提供了潜在的治疗点.
科学领域:
- 心血管研究研究心血管研究
- 代谢综合征是代谢综合征的一种.
- 分子生物学分子生物学
背景情况:
- 代谢性高血压 (MHR) 是代谢综合征的关键组成部分,显著增加心血管疾病的风险.
- 有效管理MHR是具有挑战性的,需要识别关键的致病因子和新的治疗点.
- 了解MHR背后的分子机制对于开发有针对性的干预措施至关重要.
研究的目的:
- 确定代谢性高血压 (MHR) 的致病因素和潜在的治疗点.
- 调查基特异性蛋白酶18 (USP18) 在MHR病原和其下游信号通路中的作用.
- 探索USP18对内皮细胞增殖,细胞亡和氧化应激的影响.
主要方法:
- 使用高糖,高脂肪饮食和乙醇建立了代谢高血压大鼠模型.
- 采用了他的病理学染色 (血素-素,Sirius Red),转录基因组测序和西部涂抹.
- 使用CCK-8,流细胞计和ELISAs评估USP18在HUVEC扩散,亡和氧化应激中的作用.
主要成果:
- 在MHR模型中表现出脂质不良,血管厚度增加,原沉积和氧化应激标志物.
- 转录组测序确定了78个差异表达的基因,USP18被确定为一个关键的枢纽基因.
- USP18过度表达促进了HUVEC的扩散,减少了亡和氧化应激,并抑制了JAK/STAT通路.
结论:
- 通过调节内皮细胞行为和抑制JAK/STAT通路,USP18在代谢性高血压中起着保护作用.
- USP18证明了作为缓解MHR进展和相关心血管风险的治疗目标的潜力.
- 针对USP18可以提供一种新的策略来管理代谢性高血压.
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