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Fibrin turnover and pleural organization: bench to bedside
Author(s) -
Andrey A. Komissarov,
Najib M. Rahman,
Gary Lee,
Galina Florova,
Sreerama Shetty,
Richard Idell,
Mitsuo Ikebe,
Kumuda C. Das,
Torry A. Tucker,
Steven Idell
Publication year - 2018
Publication title -
ajp lung cellular and molecular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.892
H-Index - 163
eISSN - 1522-1504
pISSN - 1040-0605
DOI - 10.1152/ajplung.00501.2017
Subject(s) - medicine , tissue plasminogen activator , plasminogen activator , intensive care medicine , bench to bedside , fibrinolytic agent , fibrin , activator (genetics) , fibrinolysis , mesothelial cell , bioinformatics , pathology , immunology , biology , medical physics , receptor
Recent studies have shed new light on the role of the fibrinolytic system in the pathogenesis of pleural organization, including the mechanisms by which the system regulates mesenchymal transition of mesothelial cells and how that process affects outcomes of pleural injury. The key contribution of plasminogen activator inhibitor-1 to the outcomes of pleural injury is now better understood as is its role in the regulation of intrapleural fibrinolytic therapy. In addition, the mechanisms by which fibrinolysins are processed after intrapleural administration have now been elucidated, informing new candidate diagnostics and therapeutics for pleural loculation and failed drainage. The emergence of new potential interventional targets offers the potential for the development of new and more effective therapeutic candidates.

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