通过MLKL介导的内皮细胞亡导致系统性炎症反应综合征的血管损伤和死亡率
Xiaoxia Wu1, Xiaoming Zhao1, Fang Li2
1CAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, PR China.
Cellular & molecular immunology
|September 30, 2024
概括
系统性炎症反应综合征 (SIRS) 的死亡率与细胞死亡途径 - - 亡有关. 向内皮细胞亡可能为SIRS和多器官功能障碍综合征 (MODS) 提供新的治疗方法.
科学领域:
- 免疫学 免疫学 免疫学
- 病理生理学 病理生理学
- 血管生物学 血管生物学
背景情况:
- 系统性炎症反应综合征 (SIRS) 通过细胞因子过分分泌导致危及生命的死亡,导致多器官功能障碍综合征 (MODS).
- 凝血病和亡都与SIRS病变产生有关,但经历亡的特定细胞类型及其与凝血病的相互关系尚不清楚.
研究的目的:
- 调查死细胞灭绝在SIRS相关死亡率中的作用及其与凝血病的关系.
- 为了确定在TNF-α诱导的SIRS中经历亡的特定细胞类型.
- 评估向SIRS中的内皮细胞亡的治疗潜力.
主要方法:
- 肠道显微镜用于小鼠的可视化分析.
- 小鼠接受了抗凝剂和非抗凝剂肝素的预治疗.
- 用基因操纵 (Mlkl或Ripk3删除) 和血统追踪 (Tie2-Cre;Rosa26-tdT) 来研究内皮细胞 (EC) 亡.
主要成果:
- 在SIRS中,抗凝血剂和非抗凝血剂赫巴林保护小鼠免受TNF-α诱导的死亡.
- 在TNF-α诱导的SIRS中,Mlkl或Ripk3的删除降低了凝血和死亡率,这表明死细胞亡在凝血之前起作用.
- 内皮细胞 (EC) 亡被确定为TNF-α治疗小鼠血管损伤的原因,其抑制可以防止致命的SIRS.
结论:
- RIPK3-MLKL依赖性亡破坏了血管完整性,导致凝血病,多器官衰竭和SIRS中的死亡.
- 针对血管EC亡是SIRS患者的一个有前途的治疗策略.
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