在急性心肌梗塞期间,失调的补体激活导致通过C5a:C5a-受体1轴的内皮糖分解和内皮功能障碍

Carl Vahldieck1,2,3, Samuel Löning2, Constantin Hamacher2

  • 1Department of Anesthesiology and Intensive Care Medicine, University Medical Centre Schleswig-Holstein Campus Luebeck, Luebeck, Germany.

PubMed
概括

在心肌梗塞期间补充C5a的激活会破坏内皮糖体,减少氧化并增加炎症. 阻断C5a受体1 (C5aR1) 可以防止这种损伤,为急性心肌梗塞提供新的治疗策略.

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