Initiation of coagulation in DIC. Pathogens, dead cells, and their derived molecular pattern molecules (PAMPs and DAMPs) can signal through PRRs to induce TF expression and microparticle release from monocytes, and to promote synthesis of proinflammatory cytokines that further amplify TF expression, thus initiating coagulation via the extrinsic pathway. In parallel, contact activation with FXIIa generation can occur on the surface of the pathogens, PAMPs, DAMPs, and cell debris. In particular, bacteria-derived long-chain polyphosphates (LC-poly-Ps) and platelet-derived short-chain polyphosphates (SC-poly-P), and the extracellular nucleic acids (DNA/RNA) can induce contact-mediated autoactivation of FXII and trigger coagulation via the intrinsic pathway. Both pathways converge into the common coagulation mechanism, leading to thrombin generation and downstream platelet activation and fibrin and thrombus formation.