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        Fibrinolysis in platelet thrombi

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        ijms_22_05135_v2.pdf (PDF, 978Kb)
        Author
        Kanji, Rahim
        Gue, Ying X.
        Memtsas, Vassilios
        Gorog, Diana
        Attention
        2299/24961
        Abstract
        The extent and duration of occlusive thrombus formation following an arterial atherothrombotic plaque disruption may be determined by the effectiveness of endogenous fibrinolysis. The determinants of endogenous fibrinolysis are the source of much research, and it is now broadly accepted that clot composition, as well as the environment in which the thrombus was formed, play a significant role. Thrombi with a high platelet content demonstrate significant resistance to fibrinolysis, and this may be attributable to an augmented ability for thrombin generation and the release of fibrinolysis inhibitors, resulting in a fibrin-dense, stable thrombus. Additional platelet activators may augment thrombin generation further, and in the case of coronary stenosis, high shear has been shown to strengthen the attachment of the thrombus to the vessel wall. Neutrophil extra cellular traps contribute to the fibrinolysis resistance. Additionally, platelet-mediated clot retraction, release of Factor XIII and resultant crosslinking with fibrinolysis inhibitors imparts structural stability to the thrombus against dislodgment by flow. Further work is needed in this rapidly evolving field, and efforts to mimic the pathophysiological environment in vitro are essential to further elucidate the mechanism of fibrinolysis resistance and in providing models to assess the effects of pharmacotherapy.
        Publication date
        2021-05-12
        Published in
        International Journal of Molecular Sciences
        Published version
        https://doi.org/10.3390/ijms22105135
        Other links
        http://hdl.handle.net/2299/24961
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