dc.contributor.author | Kanji, Rahim | |
dc.contributor.author | Gue, Ying X. | |
dc.contributor.author | Memtsas, Vassilios | |
dc.contributor.author | Gorog, Diana | |
dc.date.accessioned | 2021-08-05T15:30:01Z | |
dc.date.available | 2021-08-05T15:30:01Z | |
dc.date.issued | 2021-05-12 | |
dc.identifier.citation | Kanji , R , Gue , Y X , Memtsas , V & Gorog , D 2021 , ' Fibrinolysis in platelet thrombi ' , International Journal of Molecular Sciences (IJMS) , vol. 22 , no. 10 , 5135 . https://doi.org/10.3390/ijms22105135 | |
dc.identifier.issn | 1661-6596 | |
dc.identifier.uri | http://hdl.handle.net/2299/24961 | |
dc.description | © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/) | |
dc.description.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. | en |
dc.format.extent | 12 | |
dc.format.extent | 1002013 | |
dc.language.iso | eng | |
dc.relation.ispartof | International Journal of Molecular Sciences (IJMS) | |
dc.title | Fibrinolysis in platelet thrombi | en |
dc.contributor.institution | Centre for Health Services and Clinical Research | |
dc.contributor.institution | Basic and Clinical Science Unit | |
dc.contributor.institution | School of Life and Medical Sciences | |
dc.contributor.institution | Department of Clinical, Pharmaceutical and Biological Science | |
dc.description.status | Peer reviewed | |
rioxxterms.versionofrecord | 10.3390/ijms22105135 | |
rioxxterms.type | Journal Article/Review | |
herts.preservation.rarelyaccessed | true | |