Complement activation following oxidative stress

Complement activation following oxidative stress
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DOI:
10.1016/s0161-5890(99)00116-9
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发表时间:
1999-09-01
影响因子:
3.6
通讯作者:
Stahl, GL
Stahl, GL
中科院分区:
医学3区
文献类型:
--
作者:
Collard, CD;Lekowski, R;Stahl, GL

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内皮细胞在维持血管内环境稳定中起着不可或缺的作用。然而,与缺血组织再灌注相关的氧化应激激活补体,导致血管动态平衡的丧失和促炎状态。心肌梗死(Hill和Ward,1971)、动脉粥样硬化(Vlaicu等人,1985)、肠缺血(Fruchterman等人,1998)、失血性休克(西班牙等人,1999)、脓毒症(Lubbe等人,1994)和肺损伤(Mulrigan等人,1996)与补体激活有关。然而,氧化应激后补体激活的机制尚未完全阐明。
The endothelium plays an integral role in the maintenance of vascular homeostasis. However, oxidative stress associated with reperfusion of ischemic tissues activates complement, resulting in a loss of vascular homeostasis and a pro-inflammatory state. Complement activation following ischemia-reperfusion (I/R) is associated with myocardial infarction (Hill and Ward, 1971), atherosclerosis (Vlaicu et al., 1985), intestinal ischemia (Fruchterman et al., 1998), hemorrhagic shock (Spain et al., 1999), sepsis (Lubbe et al., 1994) and pulmonary injury (Mulligan et al., 1996). However, the mechanisms of complement activation following oxidative stress have not been fully elucidated.