{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T22:02:42Z","timestamp":1789768962775,"version":"4.0.1"},"reference-count":33,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,9,12]],"date-time":"2013-09-12T00:00:00Z","timestamp":1378944000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiovascular Therapeutics"],"published-print":{"date-parts":[[2013,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Aims<\/jats:title><jats:p>In a model of acute inflammation, <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>actor <jats:styled-content style=\"fixed-case\">X<\/jats:styled-content>a inhibitors have been reported not only to suppress the coagulation system but also to exert anti\u2010inflammatory effects. However, this has not been experimentally demonstrated in a model of chronic inflammation. Recent studies demonstrated that vascular inflammation in the metabolic syndrome plays major roles in the development of thrombotic diseases. Therefore, we examined the anti\u2010inflammatory effects of fondaparinux, a <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>actor <jats:styled-content style=\"fixed-case\">X<\/jats:styled-content>a inhibitor, in a mouse model of the metabolic syndrome, looking at both leukocyte adhesion on the vascular endothelium and thrombus formation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Following clamping of the mesenteric vein for 20\u00a0min in the <jats:styled-content style=\"fixed-case\">KK<\/jats:styled-content>\u2010A<jats:sup>y<\/jats:sup> mouse, mice were administered by subcutaneous injection either low\u2010dose or high\u2010dose fondaparinux or placebo (n\u00a0=\u00a010 in each group. Microscopic observation of the intestinal microcirculation was carried out. In another series, blood samples were taken and measured for blood cell counts and organ damage markers (n\u00a0=\u00a06 in each).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Both leukocyte adherence and thrombus formation were inhibited by treatment with fondaparinux. Red blood cell and white blood cell counts were maintained better in high\u2010dose group. Levels of alanine aminotransferase (<jats:styled-content style=\"fixed-case\">ALT<\/jats:styled-content>) were significantly reduced in both low\u2010dose and high\u2010dose groups (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05 and 0.01, compared with control, respectively).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Factor Xa inhibitor attenuates leukocyte adhesion and leukocyte\u2010platelet conjugate formation in a mouse model of the metabolic syndrome. These effects appeared to be related to both inhibition of thrombus formation and reduction in markers of organ damage.<\/jats:p><\/jats:sec>","DOI":"10.1111\/1755-5922.12018","type":"journal-article","created":{"date-parts":[[2013,5,1]],"date-time":"2013-05-01T23:06:43Z","timestamp":1367449603000},"page":"280-284","source":"Crossref","is-referenced-by-count":11,"title":["Factor <scp>X<\/scp>a Inhibitor Attenuates Leukocyte Adhesion and Thrombus Formation in an Experimental Mouse Model of the Metabolic Syndrome"],"prefix":"10.1111","volume":"31","author":[{"given":"Toshiaki","family":"Iba","sequence":"first","affiliation":[{"name":"Department of Emergency and Disaster Medicine Juntendo University Graduate School of Medicine Bunkyo\u2010ku Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koichiro","family":"Aihara","sequence":"additional","affiliation":[{"name":"Department of Emergency and Disaster Medicine Juntendo University Graduate School of Medicine Bunkyo\u2010ku Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shin","family":"Watanabe","sequence":"additional","affiliation":[{"name":"Department of Emergency and Disaster Medicine Juntendo University Graduate School of Medicine Bunkyo\u2010ku Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Youichi","family":"Yanagawa","sequence":"additional","affiliation":[{"name":"Department of Emergency and Disaster Medicine Juntendo University Graduate School of Medicine Bunkyo\u2010ku Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Atushi","family":"Yamada","sequence":"additional","affiliation":[{"name":"Department of Emergency and Disaster Medicine Juntendo University Graduate School of Medicine Bunkyo\u2010ku Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Niwa","family":"Koichiro","sequence":"additional","affiliation":[{"name":"Department of Emergency and Disaster Medicine Juntendo University Graduate School of Medicine Bunkyo\u2010ku Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akimichi","family":"Ohsaka","sequence":"additional","affiliation":[{"name":"Department of Transfusion Medicine and Stem Cell Regulation Juntendo University Graduate School of Medicine Bunkyo\u2010ku Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,9,12]]},"reference":[{"key":"e_1_2_8_2_1","first-page":"565","article-title":"Arterial endothelial dysfunction and idiopathic deep venous thrombosis","volume":"25","author":"Mazzoccoli G","year":"2011","journal-title":"J Biol Regul Homeost Agents"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.107.709204"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1053\/j.seminhematol.2007.02.004"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1538-7836.2006.02058.x"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehi018"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.thromres.2007.09.010"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa022157"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1055\/s-0029-1234140"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.3324\/haematol.10828"},{"key":"e_1_2_8_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.thromres.2007.02.005"},{"key":"e_1_2_8_12_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1538-7836.2006.02132.x"},{"key":"e_1_2_8_13_1","doi-asserted-by":"publisher","DOI":"10.3324\/haematol.2009.011866"},{"key":"e_1_2_8_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(06)68474-2"},{"key":"e_1_2_8_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jvs.2008.11.049"},{"key":"e_1_2_8_16_1","doi-asserted-by":"publisher","DOI":"10.1097\/00024382-200202000-00013"},{"key":"e_1_2_8_17_1","doi-asserted-by":"publisher","DOI":"10.1186\/cc6943"},{"key":"e_1_2_8_18_1","doi-asserted-by":"publisher","DOI":"10.2337\/diab.32.9.804"},{"key":"e_1_2_8_19_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.thromres.2012.03.001"},{"key":"e_1_2_8_20_1","doi-asserted-by":"publisher","DOI":"10.1097\/01.shk.0000228800.56223.db"},{"key":"e_1_2_8_21_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejvs.2010.09.025"},{"key":"e_1_2_8_22_1","doi-asserted-by":"publisher","DOI":"10.1160\/TH09-08-0562"},{"key":"e_1_2_8_23_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejim.2007.10.019"},{"key":"e_1_2_8_24_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.tem.2006.07.006"},{"key":"e_1_2_8_25_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa011100"},{"issue":"1","key":"e_1_2_8_26_1","first-page":"60","article-title":"Factor Xa or thrombin: is factor Xa a better target? 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