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  Indian J Med Microbiol
 

Figure 1: (a-c) Coagulation is initiated through the interaction of tissue factor, upregulated by inflammatory stimuli, with Factor VII, which generates activated Factor VIIa. The tissue factor–Factor VIIa complex then catalyses the conversion of Factor X to Factor Xa, leading consecutively to the activation of Factor V and the conversion of prothrombin to thrombin (FIIa). Thrombin then directly causes clot formation by cleaving fibrinogen to fibrin and also activates FXIII. (d) Inhibition of coagulation cascades occur through inactivation of FVa by protein S and activated protein C generated by the thrombomodulin–thrombin complex. Excess thrombin is compensated by direct inhibition by anti-thrombin III via formation of the thrombin–anti-thrombin III complex[9],[10]

Figure 1: (a-c) Coagulation is initiated through the interaction of tissue factor, upregulated by inflammatory stimuli, with Factor VII, which generates activated Factor VIIa. The tissue factor–Factor VIIa complex then catalyses the conversion of Factor X to Factor Xa, leading consecutively to the activation of Factor V and the conversion of prothrombin to thrombin (FIIa). Thrombin then directly causes clot formation by cleaving fibrinogen to fibrin and also activates FXIII. (d) Inhibition of coagulation cascades occur through inactivation of FVa by protein S and activated protein C generated by the thrombomodulin–thrombin complex. Excess thrombin is compensated by direct inhibition by anti-thrombin III via formation of the thrombin–anti-thrombin III complex<sup>[9],[10]</sup>