The Contribution of the Urokinase Plasminogen Activator and the Urokinase Receptor to Pleural and Parenchymal Lung Injury and Repair: A Narrative Review.
The Contribution of the Urokinase Plasminogen Activator and the Urokinase Receptor to Pleural and Parenchymal Lung Injury and Repair: A Narrative Review.
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DOI：
10.3390/ijms22031437
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发表时间：
2021-02-01
影响因子：
5.6
通讯作者：
Idell S
中科院分区：
文献类型：
--
作者：
Tucker TA;Idell S
长期以来，胸膜和实质肺损伤的特点是急性炎症和病理组织重组，当病情严重时。尽管移行基质沉积是损伤反应的正常部分，但未溶解的纤维蛋白沉积可导致受影响区域的胸膜循环和结节。在这篇综述中，我们简要讨论了纤溶途径，它的组成部分，以及它们对损伤进展的贡献。我们回顾了凝血增加和纤溶酶原激活物活性降低导致的局部纤溶紊乱如何促进血管外纤维蛋白沉积。此外，我们描述了胸膜间皮细胞如何通过获得促纤维化表型而促进肺瘢痕形成。我们还讨论了可溶性uPAR，一种新近发现的胸膜损伤生物标志物，以及它在胸腔积液分级中的诊断价值。最后，我们对单链尿激酶型纤溶酶原激活剂(UPA)治疗房性胸膜积液的临床重要性进行了深入的讨论。
Pleural and parenchymal lung injury have long been characterized by acute inflammation and pathologic tissue reorganization, when severe. Although transitional matrix deposition is a normal part of the injury response, unresolved fibrin deposition can lead to pleural loculation and scarification of affected areas. Within this review, we present a brief discussion of the fibrinolytic pathway, its components, and their contribution to injury progression. We review how local derangements of fibrinolysis, resulting from increased coagulation and reduced plasminogen activator activity, promote extravascular fibrin deposition. Further, we describe how pleural mesothelial cells contribute to lung scarring via the acquisition of a profibrotic phenotype. We also discuss soluble uPAR, a recently identified biomarker of pleural injury, and its diagnostic value in the grading of pleural effusions. Finally, we provide an in-depth discussion on the clinical importance of single-chain urokinase plasminogen activator (uPA) for the treatment of loculated pleural collections.
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DOI：
10.1164/ajrccm/140.4.1104
发表时间：
1989-10-01
期刊：
AMERICAN REVIEW OF RESPIRATORY DISEASE
影响因子：
--
作者：
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通讯作者：
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影响因子：
7.5
作者：
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影响因子：
4.4
作者：
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通讯作者：
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DOI：
10.1165/rcmb.2014-0168oc
发表时间：
2015-04-01
影响因子：
6.4
作者：
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通讯作者：
Komissarov, Andrey A.
影响因子：
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作者：
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