{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Poole LG"],"funding":["NIDDK NIH HHS","NHLBI NIH HHS","European Hematology Association","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["2520-2531"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8109015"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["137(18)"],"pubmed_abstract":["Intravascular fibrin clot formation follows a well-ordered series of reactions catalyzed by thrombin cleavage of fibrinogen leading to fibrin polymerization and cross-linking by factor XIIIa (FXIIIa). Extravascular fibrin(ogen) deposits are observed in injured tissues; however, the mechanisms regulating fibrin(ogen) polymerization and cross-linking in this setting are unclear. The objective of this study was to determine the mechanisms of fibrin polymerization and cross-linking in acute liver injury induced by acetaminophen (APAP) overdose. Hepatic fibrin(ogen) deposition and cross-linking were measured following APAP overdose in wild-type mice, mice lacking the catalytic subunit of FXIII (FXIII-/-), and in FibAEK mice, which express mutant fibrinogen insensitive to thrombin-mediated fibri"],"journal":["Blood"],"pubmed_title":["Factor XIII cross-links fibrin(ogen) independent of fibrin polymerization in experimental acute liver injury."],"pmcid":["PMC8109015"],"funding_grant_id":["T32 GM092715","RG41","R01 DK120289","R01 DK112778","F32 DK121423","R01 DK105099","R01 CA211098","U01 HL143403"],"pubmed_authors":["Pant A","Cline-Fedewa HM","Flick MJ","Kopec AK","Luyendyk JP","Poole LG","Groeneveld DJ","Baker KS"],"additional_accession":[]},"is_claimable":false,"name":"Factor XIII cross-links fibrin(ogen) independent of fibrin polymerization in experimental acute liver injury.","description":"Intravascular fibrin clot formation follows a well-ordered series of reactions catalyzed by thrombin cleavage of fibrinogen leading to fibrin polymerization and cross-linking by factor XIIIa (FXIIIa). Extravascular fibrin(ogen) deposits are observed in injured tissues; however, the mechanisms regulating fibrin(ogen) polymerization and cross-linking in this setting are unclear. The objective of this study was to determine the mechanisms of fibrin polymerization and cross-linking in acute liver injury induced by acetaminophen (APAP) overdose. Hepatic fibrin(ogen) deposition and cross-linking were measured following APAP overdose in wild-type mice, mice lacking the catalytic subunit of FXIII (FXIII-/-), and in FibAEK mice, which express mutant fibrinogen insensitive to thrombin-mediated fibri","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 May","modification":"2025-04-04T10:16:31.633Z","creation":"2025-04-04T10:16:31.633Z"},"accession":"S-EPMC8109015","cross_references":{"pubmed":["33569603"],"doi":["10.1182/blood.2020007415"]}}