Blood coagulation as an intrinsic pathway for proinflammation: a mini review.
Blood coagulation could be recognized as intrinsic inflammation. The coagulant mediators (FVIIa, FXa, thrombin (FIIa), FXIIa) and fibrin(ogen) activate cellular signaling, eliciting the production of cytokines, chemokines, growth factors, and other proinflammatory mediators. Hypercoagulability with elevated coagulant mediators would certainly trigger hyper-inflammatory state not to mention about the direct hypercoagulable actions on thrombosis, and platelet and complement activations, all of which contribute to inflammatory events. Furthermore, anticoagulant's anti-inflammatory effects readily reinforce the proposal that blood coagulation results in inflammation. The observations on protease activated receptor (PAR) activation and PAR antagonists modulating inflammation are also in line with the concept of coagulation-dependent inflammation.
Chu
Arthur J
AJ
Biological & Physical Sciences, Delta State University, Cleveland, MS 38733. USA. achu@deltastate.edu
D000818:Animals; D001777:Blood Coagulation; D001779:Blood Coagulation Factors / Q000037:antagonists & inhibitors / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000188:drug therapy / Q000378:metabolism; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051379:Mice; D019851:Thrombophilia / Q000097:blood / Q000150:complications*
D001779:Blood Coagulation Factors; D018836:Inflammation Mediators