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血液溶解相关的血栓炎症和免疫失调的基本机制
Jordan D Dimitrov1, Lubka T Roumenina1, Gina Perrella2
1Centre de Recherche des Cordeliers, INSERM, CNRS, Sorbonne Université, Université de Paris, Centre de Recherche des Cordeliers, France (J.D.D., L.T.R.).
Arteriosclerosis, thrombosis, and vascular biology
|June 15, 2023
概括
溶血性疾病通过释放无细胞血红素,这是器官损伤的强有力的触发因素,导致血栓形成和炎症. 本综述详细介绍了血红素如何驱动这些有害的血栓炎症状态,并影响感染反应.
科学领域:
- 血液学 血液学 血液学
- 免疫学 免疫学 免疫学
- 病理生理学 病理生理学
背景情况:
- 血液溶解性疾病,无论原因如何,都与血栓形成,炎症和免疫失调有关,导致器官损伤和不良预后.
- 红细胞的破坏 (血液溶解) 释放了与损伤相关的分子模式 (DAMP),如腺二酸盐 (ADP),血红蛋白和血红素.
- 这些DAMP激活多个受体和信号通路,促进一种亲炎性和亲血栓性状态.
研究的目的:
- 审查血液溶解和细胞外血红素导致血栓炎症状态的机制.
- 讨论血液溶解对宿主对二次感染的反应的影响.
主要方法:
- 文献综述侧重于血液溶解诱导的炎症和血栓形成的分子和细胞机制.
- 分析特定的损伤相关分子模式 (DAMPs) 的作用,特别是细胞外血.
- 检查对宿主防御感染的影响.
主要成果:
- 细胞外自由血红 acting作为一个警报剂,启动氧化炎症和血栓事件.
- 血红素激活血小板,内皮细胞,先天性免疫细胞,以及凝血和补充级联.
- 血液溶解加剧了宿主对二次感染的脆弱性.
结论:
- 血液溶解是由像血红蛋白这样的DAMP驱动的,建立了一个有害的血栓炎症环境.
- 了解这些机制对于管理血液溶解性疾病及其并发症,包括感染易感性至关重要.
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