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Coagulation
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===Regulators=== [[File:Coagulation full.svg|400px|thumb|right|Coagulation with arrows for negative and positive feedback.]] Several mechanisms keep platelet activation and the coagulation cascade in check.<ref name="Dicks24">{{Cite journal |last=Dicks |first=AB |last2=Moussallem |first2=E |last3=Stanbro |first3=M |last4=Walls |first4=J |last5=Gandhi |first5=S |last6=Gray |first6=BH |date=9 January 2024 |title=A Comprehensive Review of Risk Factors and Thrombophilia Evaluation in Venous Thromboembolism. |journal=Journal of Clinical Medicine |volume=13 |issue=2 |page=362 |doi=10.3390/jcm13020362 |pmc=10816375 |pmid=38256496 |doi-access=free}}</ref> Abnormalities can lead to an increased tendency toward thrombosis: ====Protein C and Protein S==== [[Protein C]] is a major physiological anticoagulant. It is a vitamin K-dependent [[Serine protease|serine protease enzyme]] that is activated by thrombin into activated protein C (APC). Protein C is activated in a sequence that starts with Protein C and thrombin binding to a cell surface protein [[thrombomodulin]]. Thrombomodulin binds these proteins in such a way that it activates Protein C. The activated form, along with [[protein S]] and a phospholipid as cofactors, degrades FVa and FVIIIa. Quantitative or qualitative deficiency of either (protein C or protein S) may lead to [[thrombophilia]] (a tendency to develop thrombosis). Impaired action of Protein C (activated Protein C resistance), for example by [[Factor V Leiden|having the "Leiden" variant of Factor V]] or high levels of FVIII, also may lead to a thrombotic tendency.<ref name=Dicks24/> ====Antithrombin==== [[Antithrombin]] is a [[serine protease inhibitor]] ([[serpin]]) that degrades the serine proteases: thrombin, FIXa, FXa, FXIa, and FXIIa. It is constantly active, but its adhesion to these factors is increased by the presence of [[heparan sulfate]] (a [[glycosaminoglycan]]) or the administration of [[heparin]]s (different heparinoids increase affinity to FXa, thrombin, or both). Quantitative or qualitative deficiency of antithrombin (inborn or acquired, e.g., in [[proteinuria]]) leads to thrombophilia.<ref name=Dicks24/> ====Tissue factor pathway inhibitor (TFPI)==== [[Tissue factor pathway inhibitor]] (TFPI) limits the action of tissue factor (TF). It also inhibits excessive TF-mediated activation of FVII and FX.<ref>{{Cite journal |vauthors=Maroney SA, Mast AE |date=June 2015 |title=New insights into the biology of tissue factor pathway inhibitor |journal=J Thromb Haemost |volume=13 |issue=Suppl 1 |pages=S200β07 |doi=10.1111/jth.12897 |pmc=4604745 |pmid=26149025}}</ref> ====Plasmin==== [[Plasmin]] is generated by proteolytic cleavage of plasminogen, a plasma protein synthesized in the liver. This cleavage is catalyzed by [[tissue plasminogen activator]] (t-PA), which is synthesized and secreted by endothelium. Plasmin proteolytically cleaves fibrin into fibrin degradation products that inhibit excessive fibrin formation.{{citation needed|date=June 2022}} ====Prostacyclin==== [[Prostacyclin]] (PGI<sub>2</sub>) is released by endothelium and activates platelet G<sub>s</sub> protein-linked receptors. This, in turn, activates [[adenylyl cyclase]], which synthesizes cAMP. cAMP inhibits platelet activation by decreasing cytosolic levels of calcium and, by doing so, inhibits the release of granules that would lead to activation of additional platelets and the coagulation cascade.<ref name="Hoffbrand">{{Cite book |last=Hoffbrand |first=A.V. |title=Essential haematology |publisher=Blackwell Science |year=2002 |isbn=978-0-632-05153-3 |location=Oxford |pages=243β45}}</ref>
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