动脉样硬化中的巨极化和炎症机制:对预防和治疗的影响
Bo Yang1, Sanhua Hang2, Siting Xu1
1Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China.
Heliyon
|June 14, 2024
概括
这篇评论探讨了M1巨细胞如何在动脉样硬化中驱动炎症. 它探讨了代谢变化和针对巨细胞的治疗策略,以预防和治疗这种心血管疾病.
科学领域:
- 心血管研究研究心血管研究
- 免疫学 免疫学 免疫学
- 代谢疾病 代谢疾病
背景情况:
- 动脉样硬化是一种由斑块积聚引起的慢性炎症性动脉疾病.
- 大细胞起着至关重要的作用,M1表型促进炎症,M2表型抵消炎症.
研究的目的:
- 审查影响动脉样硬化的M1巨分化因素.
- 探索M1巨细胞的代谢重编程和细胞因子分泌.
- 讨论针对巨细胞和炎症通路的新兴治疗策略.
主要方法:
- 文献综述侧重于动脉样硬化中M1巨细胞极化.
- 对代谢重编程和细胞因子分泌机制的分析.
- 检查当前和新的治疗干预措施.
主要成果:
- 超脂血症诱导的修饰性脂蛋白促进M1巨细胞的招募和激活.
- 巨细胞吞脂质,形成泡细胞,这些细胞有助于死斑核.
- M1巨细胞分泌有助于炎症的细胞因子,加剧动脉样硬化进展.
结论:
- 了解M1巨细胞两极分化是动脉样硬化病原体的关键.
- 向巨细胞表型和炎症途径提供了有前途的治疗途径.
- 类药物,PCSK9抑制剂和纳米向药物显示出动脉样硬化治疗的潜力.
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