Fibrinolysis in Platelet Thrombi

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 subject of much research, and it is now broadly accepted that clot c...

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Bibliographic Details
Published in:International journal of molecular sciences 2021-05, Vol.22 (10), p.5135
Main Authors: Kanji, Rahim, Gue, Ying X., Memtsas, Vassilios, Gorog, Diana A.
Format: Article
Language:English
Subjects:
Blood clots
Blood platelets
clot retraction
clot stability
Coagulation factors
Crosslinking
Drug therapy
Factor XIII
Fibrin
Fibrinolysis
Flow stability
Glycoproteins
Heart attacks
Inhibitors
Leukocytes (neutrophilic)
Microscopy
Morphology
Neutrophils
Review
shear
Shear stress
Stenosis
Structural stability
Thrombin
Thrombosis
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Summary: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 subject 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 extracellular traps contribute to fibrinolysis resistance. Additionally, platelet-mediated clot retraction, release of Factor XIII and resultant crosslinking with fibrinolysis inhibitors impart 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.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms22105135