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.

心脏病发作造成的损伤程度是预后和生存的主要决定因素。被阻塞的动脉的大小以及在心脏病发作后再次打开的速度是决定损伤程度的重要因素。然而，现在很清楚，另一种形式的损伤也会发生，矛盾的是，在血液供应恢复的时候。这就是所谓的缺血再灌注损伤。这种类型的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激活血液中称为补体系统的系统起作用。我们已经开发了一种独特的模型来研究这一通路在缺血再灌注损伤中的作用。拟议的研究将提供关于该途径在引起缺血再灌注损伤中的重要性以及抑制该系统是否是心脏病发作后保护心脏的有价值的方法的明确信息。