{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T03:03:00Z","timestamp":1790910180580,"version":"4.1.0"},"reference-count":96,"publisher":"MDPI AG","issue":"10","license":[{"start":{"date-parts":[[2021,5,12]],"date-time":"2021-05-12T00:00:00Z","timestamp":1620777600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>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.<\/jats:p>","DOI":"10.3390\/ijms22105135","type":"journal-article","created":{"date-parts":[[2021,5,12]],"date-time":"2021-05-12T22:46:14Z","timestamp":1620859574000},"page":"5135","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Fibrinolysis in Platelet Thrombi"],"prefix":"10.3390","volume":"22","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9801-259X","authenticated-orcid":false,"given":"Rahim","family":"Kanji","sequence":"first","affiliation":[{"name":"Faculty of Medicine, National Heart and Lung Institute, Imperial College, London SW3 6LY, UK"},{"name":"Cardiology Department, East and North Hertfordshire NHS Trust, Stevenage, Hertfordshire SG1 4AB, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9994-8915","authenticated-orcid":false,"given":"Ying X.","family":"Gue","sequence":"additional","affiliation":[{"name":"Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart &amp; Chest Hospital, Liverpool L69 7TX, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vassilios","family":"Memtsas","sequence":"additional","affiliation":[{"name":"Cardiology Department, East and North Hertfordshire NHS Trust, Stevenage, Hertfordshire SG1 4AB, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9286-1451","authenticated-orcid":false,"given":"Diana A.","family":"Gorog","sequence":"additional","affiliation":[{"name":"Faculty of Medicine, National Heart and Lung Institute, Imperial College, London SW3 6LY, UK"},{"name":"Cardiology Department, East and North Hertfordshire NHS Trust, Stevenage, Hertfordshire SG1 4AB, UK"},{"name":"School of Life and Medical Sciences, Postgraduate Medical School, University of Hertfordshire, Hatfield AL10 9AB, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2021,5,12]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"295","DOI":"10.1093\/eurheartj\/ehy656","article-title":"Impaired endogenous fibrinolysis in ST-segment elevation myocardial infarction patients undergoing primary percutaneous coronary intervention is a predictor of recurrent cardiovascular events: The RISK PPCI study","volume":"40","author":"Farag","year":"2019","journal-title":"Eur. 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