The role of the lectin pathway of complement activation in cardiac ischemia-reperfusion injury

补体激活凝集素途径在心脏缺血再灌注损伤中的作用

• 批准号: G0700859/1
• 负责人: Wilhelm Schwaeble
• 金额: $ 50.97万
• 依托单位: University of Leicester
• 依托单位国家: 英国
• 项目类别: Research Grant
• 财政年份: 2008
• 资助国家: 英国
• 起止时间: 2008 至 无数据
• 项目状态: 已结题
• 来源: https://gtr.ukri.org/projects?ref=G0700859%2F1
• 关键词: role; lectin; pathway; complement; activation

The amount of injury caused by heart attacks is the main determinant of outcome and survival. The size of the artery that is blocked and how quickly it is opened again after the onset of the heart attack is an important factor in determining the amount of injury. However, it is now clear that another form of injury also occurs, paradoxically at the time when the blood supply is restored. This is called ischaemia-reperfusion injury. The precise cause of this type of injury is not known although there is evidence that activation of a system in the blood called the complement system by a pathway called the lectin pathway plays a role. We have developed a unique model to investigate the role of this pathway in ischaemia-reperfusion injury. The proposed studies will provide definitive information on the importance of this pathway in causing ischaemia-reperfusion injury and whether inhibiting this system would be valuable way of protecting the heart after heart attacks.

心脏病发作引起的伤害量是结果和生存的主要决定因素。心脏病发作发作后再次打开动脉的大小以及它再次打开的速度是确定损伤量的重要因素。但是，现在很明显，在恢复血液供应时，矛盾的是另一种形式的伤害。这称为缺血 - 再灌注损伤。这种损伤的确切原因尚不清楚，尽管有证据表明，通过称为凝集素途径的途径的血液中一种称为补体系统的系统激活起作用。我们已经开发了一个独特的模型来研究该途径在缺血再灌注损伤中的作用。拟议的研究将提供有关该途径在造成缺血 - 再灌注损伤的重要性的明确信息，以及在心脏病发作后抑制该系统是否是保护心脏的宝贵方式。