Model‐dependentcontributionsofFXIIandFXItovenousthrombosisinmiceJTHROMBHAEMOSTArticleNov01,:18(11),-./jth.本文由“天纳”临床学术信息人工智能系统自动翻译点击文末“阅读原文”下载本文PDFBackgroundTheintrinsicpathwayfactors(F)XIIandFXIhavebeenshowntocontributetothrombosisinanimalmodels.WeassessedtheroleofFXIIandFXIinvenousthrombosisinthreedistinctmousemodels.在动物模型中，内源性通路因子（F）XII和FXI被证明与血栓形成有关。我们在三种不同的小鼠模型中评估了FXII和FXI在静脉血栓形成中的作用。MethodsVenousthrombosiswasassessedinmicegeneticallydeficientforeitherFXIIorFXI.Threemodelswereused:theinferiorvenacava(IVC)stasis,IVCstenosis,andfemoralveinelectrolyticinjurymodels.静脉血栓形成在基因缺陷的小鼠FXII或FXI中被评估。采用三种模型：下腔静脉淤血模型、下腔静脉狭窄模型和股静脉电解损伤模型。ResultsIntheIVCstasismodel,FXIIandFXIdeficiencydidnotaffectthesizeofthrombibuttheirabsencewasassociatedwithdecreasedlevelsoffibrin(ogen)andanincreasedleveloftheneutrophilextracellulartrapmarkercitrullinatedhistoneH3.Incontrast,adeficiencyofeitherFXIIorFXIresultedinasignificantandequivalentreductioninthrombusweightandincidenceofthrombusformationintheIVCstenosismodel.ThrombiformedintheIVCstenosismodelcontainedsignificantlyhigherlevelsofcitrullinatedhistoneH3
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