{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T08:56:39Z","timestamp":1768467399601,"version":"3.49.0"},"reference-count":52,"publisher":"Georg Thieme Verlag KG","issue":"05","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Thromb Haemost"],"published-print":{"date-parts":[[2013]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Emerging evidence indicates that various haemostatic components can regulate the progression of liver disease. Thrombin-activatable fibrinolysis inhibitor (TAFI) possesses anti-inflammatory properties besides its anti-fibrinolytic function. Here, we investigated the contribution of TAFI to the progression of disease in murine models of chronic and acute liver failure. Chronic carbon tetrachloride (CCL4) administration induced liver damage and fibrosis both in TAFI knockout (TAFI\u2212\/\u2212) mice and wild-type controls. Smooth muscle actin-\u03b1 (\u03b1-SMA) content of liver tissue was significantly increased after 1 and 3 weeks, and pro-collagen \u03b11 expression was significantly increased after 3 and 6 weeks in TAFI\u2212\/\u2212 mice. TAFI\u2212\/\u2212 mice showed significantly elevated levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) after 3 weeks of CCL4. Neutrophil influx was significantly increased in TAFI\u2212\/\u2212 mice after 6 weeks of CCL4. No difference in hepatic fibrin deposition between TAFI\u2212\/\u2212 and wild-types was observed. After acetaminophen intoxication, necrosis was significantly increased in TAFI\u2212\/\u2212 mice at 24 hours (h) after injection. AST and ALT levels were decreased at 2 and 6 h after acetaminophen injection in TAFI\u2212\/\u2212 mice, but were significantly higher in the TAFI\u2212\/\u2212 mice at 24 h. Similarly, hepatic fibrin deposition was decreased at 6 h in TAFI\u2212\/\u2212 mice, but was comparable to wild-types at 24 h after injection. In conclusion, TAFI deficiency results in accelerated fibrogenesis and increased liver damage in murine models of chronic and acute liver disease, which may be related to increased inflammation.<\/jats:p>","DOI":"10.1160\/th12-12-0930","type":"journal-article","created":{"date-parts":[[2013,3,7]],"date-time":"2013-03-07T13:14:40Z","timestamp":1362662080000},"page":"948-955","source":"Crossref","is-referenced-by-count":19,"title":["TAFI deficiency promotes liver damage in murine models of liver failure through defective down-regulation of hepatic inflammation"],"prefix":"10.1160","volume":"109","author":[{"given":"Greg C. G.","family":"Hugenholtz","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joost C. 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