Blood Coagulation as an Intrinsic Pathway for Proinflammation: A Mini Review

Author(s): Arthur J. Chu

Journal Name: Inflammation & Allergy - Drug Targets (Discontinued)
Formerly Current Drug Targets - Inflammation & Allergy

Volume 9 , Issue 1 , 2010


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, anticoagulants antiinflammatory 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.

Keywords: Blood coagulation, hypercoagulability, tissue factor, coagulant mediator, anticoagulant, inflammation, cytokines, protease-activated receptors, complement, thrombosis, cardioprotection

promotion: free to download

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2010
Page: [32 - 44]
Pages: 13
DOI: 10.2174/187152810791292890

Article Metrics

PDF: 36