Coagulation-dependent mechanisms and asthma.
Coagulation-dependent mechanisms and asthma.
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DOI：
10.1172/jci22288
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发表时间：
2004-07
期刊：
影响因子：
--
通讯作者：
M. Matthay;J. Clements
中科院分区：
文献类型：
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作者：
M. Matthay;J. Clements
在一些临床疾病中，炎症依赖性组织损伤与凝血酶形成、纤维蛋白沉积和纤维蛋白溶解受损之间存在相互作用。来自过敏性气道高反应性小鼠模型的新证据表明，凝血和纤维蛋白溶解紊乱可能有助于哮喘的发病机制。导致气道平滑肌收缩和气道高反应性的炎症机制可能与可导致气道关闭的血管外纤维蛋白、血浆渗出物和炎症细胞的积累有关。
In several clinical disorders, there are interactions between inflammation-dependent tissue injury and thrombin formation, fibrin deposition, and impaired fibrinolysis. New evidence generated from a mouse model of allergic airway hyperreactivity suggests that disordered coagulation and fibrinolysis may contribute to the pathogenesis of asthma. The inflammatory mechanisms that lead to airway smooth muscle contraction and airway hyperresponsiveness may be associated with accumulation of extravascular fibrin, plasma exudates, and inflammatory cells that can lead to airway closure.