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Coagulation and fibrinolysis in human acute lung injury--new therapeutic targets?
Journal article   Open access   Peer reviewed

Coagulation and fibrinolysis in human acute lung injury--new therapeutic targets?

Lorraine B Ware, Julie A Bastarache and Ling Wang
Keio journal of medicine, Vol.54(3), pp.142-149
09/2005
DOI: 10.2302/kjm.54.142
PMID: 16237276
url
https://doi.org/10.2302/kjm.54.142View
Published (Version of record) Open Access

Abstract

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common, life-threatening causes of acute respiratory failure that arise from a variety of local and systemic insults. The need for new specific therapies has led a number of investigators to examine the role of altered coagulation and fibrinolysis in the pathogenesis of ALI/ARDS. This review summarizes our current understanding of coagulation and fibrinolysis in human ALI/ARDS with an emphasis on pathways that could be potential therapeutic targets including the tissue factor pathway, the protein C pathway and modulation of fibrinolysis via plasminogen activator inhibitor-1. The available data suggest that clinical ALI and ARDS are characterized by profound alterations in both systemic and intra-alveolar coagulation and fibrinolysis. Fibrin deposition in the airspaces and lung microvasculature likely results from both activation of the coagulation cascade and impaired fibrinolysis, triggered by inflammation. Modulation of fibrin deposition in the lung through targeting activation and modulation of coagulation as well as fibrinolysis may be an important therapeutic target in clinical ALI/ARDS that deserves further exploration.
Blood Coagulation Fibrinolysis Humans Lipoproteins - metabolism Plasminogen Activator Inhibitor 1 - metabolism Plasminogen Activators - metabolism Protein C - metabolism Respiratory Distress Syndrome, Adult - blood Respiratory Distress Syndrome, Adult - therapy Thrombomodulin - metabolism Thromboplastin - metabolism

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