Factor XI deficiency protects against atherogenesis in Apolipoprotein E/Factor XI double knockout mice

Reut Shnerb Ganor, Dror Harats, Ginette Schiby, David Gailani, Hanna Levkovitz, Camila Avivi, Ilia Tamarin, Aviv Shaish, Ophira Salomon

Research output: Contribution to journalArticlepeer-review


Objective - Atherosclerosis and atherothrombosis are still major causes of mortality in the Western world, even after the widespread use of cholesterol-lowering medications. Recently, an association between local thrombin generation and atherosclerotic burden has been reported. Here, we studied the role of factor XI (FXI) deficiency in the process of atherosclerosis in mice. Approach and Results - Apolipoprotein E/FXI double knockout mice, created for the first time in our laboratory. There was no difference in cholesterol levels or lipoprotein profiles between apolipoprotein E knockout and double knockout mice. Nevertheless, in 24-week-old double knockout mice, the atherosclerotic lesion area in the aortic sinus was reduced by 32% (P=0.004) in comparison with apolipoprotein E knockout mice. In 42-week-old double knockout mice, FXI deficiency inhibited atherosclerosis progression significantly in the aortic sinus (25% reduction, P=0.024) and in the aortic arch (49% reduction, P=0.028), with a prominent reduction of macrophage infiltration in the atherosclerotic lesions. Conclusions - FXI deprivation was shown to slow down atherogenesis in mice. The results suggest that the development of atherosclerosis can be prevented by targeting FXI.

Original languageEnglish
Pages (from-to)475-481
Number of pages7
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Issue number3
StatePublished - 1 Mar 2016


  • atherosclerosis
  • factor XI


Dive into the research topics of 'Factor XI deficiency protects against atherogenesis in Apolipoprotein E/Factor XI double knockout mice'. Together they form a unique fingerprint.

Cite this