ABSTRACT
Abnormalities of pathways of brin turnover and aberrant extravascular brin deposition characterize pleural injury and repair. Pleural adhesions that bridge the visceral
and parietal pleural surfaces are brinous and undergo remodeling with subsequent brotic repair. Transitional brin that coats the surface of the lung can likewise undergo scarication leading to restrictive lung sequellae. As in other organ systems, the pathogenesis of pleural brosis recapitulates events associated with the progression of brotic repair during wound healing.1 Among several pathways associated with innate immunity and tissue repair, procoagulant and
Overview: The pathogenesis of pleural fibrosis and disordered fibrin turnover 67
Linkage between disordered fibrin turnover and fibrosis 68 Coagulation and pleural injury 68 Fibrinolysis and pleural injury 69 Regulation of uPA, uPAR, and PAI-1 by the
mesothelium 71 Mesomesenchymal transition (MT) in the
pathogenesis of pleual injury 71
Peripheral lung injury and the regulation of the fibrinolytic system: Ramifications for pleural fibrosis 72
Clinical applications of intrapleural fibrinolysins for the treatment of pleural loculation and impaired pleural drainage 73
The current state of intrapleural fibrinolytic therapy: Challenges and opportunities74
References 75
brinolytic systems are locally altered in pleural injury and assume special importance in its outcome. Complex interactions between coagulation, brinolysis, and other proin-ammatory pathways contribute to the remodeling process and pleural brosis.
