{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,24]],"date-time":"2026-01-24T07:17:25Z","timestamp":1769239045222,"version":"3.49.0"},"reference-count":55,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2007,8,29]],"date-time":"2007-08-29T00:00:00Z","timestamp":1188345600000},"content-version":"vor","delay-in-days":89,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of the New York Academy of Sciences"],"published-print":{"date-parts":[[2007,6]]},"abstract":"<jats:p><jats:bold><jats:sc>Abstract<\/jats:sc>:\u2002<\/jats:bold>  <jats:bold>During recent years it has become evident that atherosclerosis is an inflammatory disease. Furthermore, immune reactions and especially autoimmunity, were demonstrated to modulate atherosclerosis in animal experiments. An interesting example of how autoimmune reactions can influence atherosclerosis and consequences thereafter, is systemic lupus erythematosus (SLE)\u2010associated cardiovascular disease (CVD). Antithrombotic effect exerted by Annexin A5 (ANXA5) is thought to be mediated mainly by forming a mechanical shield over phospholipids (PLs) reducing availability of PLs for coagulation reactions. However, more specific properties of ANXA5 might be of importance for its antithrombotic function. Such examples include downregulation of surface\u2010expressed tissue factor (TF), as well as upregulation of urokinase\u2010type plasminogen activator (uPA) by ANXA5. Also, interaction of ANXA5 with ligands involved in hemostasis, such as sulfatide and heparin, has been demonstrated. We have recently described a novel mechanism potentially contributing to atherothrombosis in SLE, with ANXA5 binding to endothelium decreased in SLE, an effect caused by antiphospholipid antibodies (aPL). It may be hypothesized that ANXA5 can be effective as a treatment to prevent plaque rupture and atherothrombosis not only in SLE, but also in the general population prone to CVD. Antiatherothrombotic potential of ANXA5 deserves further attention and careful studies as the mechanism behind the majority of clinically significant cardiovascular ischemic disease is atherothrombosis, formed on an underlying vulnerable atherosclerotic lesion. It may be hypothesized that ANXA5 can be effective as a treatment to prevent plaque rupture and atherothrombosis not only in SLE, but also in a general population prone to CVD.<\/jats:bold> <\/jats:p>","DOI":"10.1196\/annals.1422.011","type":"journal-article","created":{"date-parts":[[2007,10,16]],"date-time":"2007-10-16T22:43:07Z","timestamp":1192574587000},"page":"96-103","source":"Crossref","is-referenced-by-count":40,"title":["Annexin A5 as a Novel Player in Prevention of Atherothrombosis in SLE and in the General Population"],"prefix":"10.1111","volume":"1108","author":[{"given":"ANNA","family":"CEDERHOLM","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"JOHAN","family":"FROSTEGA\u02daRD","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2007,8,29]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.59.1.13"},{"key":"e_1_2_6_3_2","first-page":"S8","article-title":"Thrombolytic, antithrombin, and antiplatelet treatment of acute coronary syndromes","volume":"100","author":"Puma J.A.","year":"2000","journal-title":"J. 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