IL-37-Smad3对ox-LDL诱导的内皮细胞功能障碍的多重保护作用
Changyi Zhang1, Xiaojun Huang1, Bin Xie1
1Department of Cardiology, Second Affiliated Hospital of Shantou University Medical College, Shantou City, Guangdong province, China.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
|February 15, 2024
概括
干白素-37 (IL-37) 通过减少内细胞网膜应激 (ERS) 和由氧化低密度脂蛋白 (ox-LDL) 引起的自,减轻动脉样硬化. 这种保护作用是通过与Smad3的结合来实现的,这提供了一个潜在的治疗策略.
科学领域:
- 心血管生物学 心血管生物学
- 免疫学 免疫学 免疫学
- 细胞应激反应的应激反应
背景情况:
- 动脉样硬化是一种由氧化低密度脂蛋白 (ox-LDL) 驱动的炎症性动脉疾病.
- 氧化LDL通过内细胞网膜应激 (ERS) 诱导内皮功能障碍.
- 众所周知,互白素-37 (IL-37) 具有血管保护功能.
研究的目的:
- 调查IL-37是否可以减轻ox-LDL诱导的ERS和自.
- 探索IL-37作为动脉样硬化的治疗剂的潜力.
主要方法:
- 使用的老鼠冠状动脉内皮细胞 (RCAECs) 用ox-LDL和IL-37治疗.
- 评估了伤口愈合率,骨质生成因子的表达和ERS通路蛋白.
- 采用Smad3静音和电子显微镜来检查IL-37/Smad3复合物的作用.
主要成果:
- 在RCAEC中,IL-37减轻了牛LDL诱导的伤口愈合率的增加.
- IL-37降低了ox-LDL诱导的亲骨质性反应,ERS和自.
- 这些效应依赖于Smad3,因为沉默Smad3取消了保护性反应.
- 电子显微镜证实IL-37/Smad3复合物抑制了内细胞网膜自.
结论:
- 通过抑制ERS和自,IL-37可以缓解由ox-LDL诱导的内皮功能障碍.
- 这种保护机制涉及IL-37/Smad3复合体.
- IL-37显示出作为动脉样硬化多重保护性治疗剂的潜力.
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