Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Apr 24;10:409. doi: 10.3389/fneur.2019.00409

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2019 Ziliotto, Bernardi, Jakimovski and Zivadinov.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Schematic representation of the coagulation cascade and fibrinolytic pathway after blood-brain barrier damage. The coagulation cascade is activated (1) when the TF binds to its ligand, (activated) factor (F)VII, thus forming, together with membranes, a mature active binary complex (TF:FVIIa). The TF:FVIIa complex allows to cleave and activate on one side FIX and on another FX (2). TF:FVIIa:FXa is able to activate the cofactor FVIII (3) which forms a complex with the FIXa (FIXa:FVIIIa) providing a feedback loop for FX activation. The assembly FXa:FVa, converts prothrombin (FII) into thrombin (FIIa) (4). The initial amount of thrombin exerts its proteolytic action on FXI, FV, FVIII, and other substrates (5). Then the massive thrombin generation reaches a sufficient concentration to convert fibrinogen (FI) into fibrin monomers (6). The organized three-dimensional assembly of monomers in protofibrils and fibrin fibers produces the blood clot. Cross-linking stabilization of fibrin clot requires FXIII activated (FXIIIa) by thrombin activity. Coagulation complexes depend on lipids, exemplified by the platelet membrane. The dissolution of the fibrin fibers is mediated by the fibrinolytic system (7). Tissue-type plasminogen activator (tPA) converts plasminogen into plasmin which cleaves fibrin to soluble degradation products among those the D-dimers.