Bench to bedside: targeting coagulation and fibrinolysis in acute lung injury.
Substantial progress has been made in understanding the contribution of alterations in coagulation and fibrinolysis to the pathogenesis of acute lung injury (ALI). Findings from mouse, rat, baboon, and human studies indicate that alterations in coagulation and fibrinolysis may be of major pathogenetic importance in ALI and other inflammatory conditions in the lung including pneumonia, sepsis, and ventilator-induced lung injury. Therapies targeted at both activation of coagulation through the extrinsic coagulation cascade and modulation of coagulation through the protein C system have the potential to favorably impact clinical ALI/acute respiratory distress syndrome.
Ware
Lorraine B
LB
Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA. lorraine.ware@vanderbilt.edu
Camerer
Eric
E
Welty-Wolf
Karen
K
Schultz
Marcus J
MJ
Matthay
Michael A
MA
D000818:Animals; D001777:Blood Coagulation / Q000276:immunology; D004195:Disease Models, Animal; D005342:Fibrinolysis / Q000276:immunology; D006801:Humans; D018448:Models, Immunological; D010215:Papio; D011014:Pneumonia / Q000097:blood; D011486:Protein C / Q000378:metabolism / Q000627:therapeutic use; D044462:Receptors, Proteinase-Activated / Q000502:physiology; D012121:Respiration, Artificial; D012128:Respiratory Distress Syndrome / Q000097:blood* / Q000276:immunology / Q000628:therapy; D018805:Sepsis / Q000378:metabolism; D018180:Thrombomodulin / Q000097:blood; D013925:Thromboplastin / Q000378:metabolism
D011486:Protein C; D044462:Receptors, Proteinase-Activated; D018180:Thrombomodulin; D013925:Thromboplastin