Evidence map›Paper›PMID 26800563›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2016

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

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.4field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Reporting Sex and Sex Differences in Preclinical Studies.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  17. Proteases, Protease-Activated Receptors, and Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  18. The coagulation system in atherothrombosis: Implications for new therapeutic strategies.Research and practice in thrombosis and haemostasis · 2018
    Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Reut Shnerb GanorFrom the The Bert W. Strassburger Lipid Center (R.S.G., D.H., H.L., A.S.) and Department of Pathology (G.S., C.A.), and Thrombosis Unit (R.S.G., I.T., O.S.), Sheba Medical Center, Tel-Hashomer, Israel; Sackler Faculty of Medicine (R.S.G., D.H., G.S., H.L., C.A., I.T., O.S.), Tel-Aviv University, Tel-Aviv, Israel; and Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN (D.G.).
Dror HaratsFrom the The Bert W. Strassburger Lipid Center (R.S.G., D.H., H.L., A.S.) and Department of Pathology (G.S., C.A.), and Thrombosis Unit (R.S.G., I.T., O.S.), Sheba Medical Center, Tel-Hashomer, Israel; Sackler Faculty of Medicine (R.S.G., D.H., G.S., H.L., C.A., I.T., O.S.), Tel-Aviv University, Tel-Aviv, Israel; and Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN (D.G.).
Ginette SchibyFrom the The Bert W. Strassburger Lipid Center (R.S.G., D.H., H.L., A.S.) and Department of Pathology (G.S., C.A.), and Thrombosis Unit (R.S.G., I.T., O.S.), Sheba Medical Center, Tel-Hashomer, Israel; Sackler Faculty of Medicine (R.S.G., D.H., G.S., H.L., C.A., I.T., O.S.), Tel-Aviv University, Tel-Aviv, Israel; and Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN (D.G.).
David GailaniFrom the The Bert W. Strassburger Lipid Center (R.S.G., D.H., H.L., A.S.) and Department of Pathology (G.S., C.A.), and Thrombosis Unit (R.S.G., I.T., O.S.), Sheba Medical Center, Tel-Hashomer, Israel; Sackler Faculty of Medicine (R.S.G., D.H., G.S., H.L., C.A., I.T., O.S.), Tel-Aviv University, Tel-Aviv, Israel; and Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN (D.G.).
Hanna LevkovitzFrom the The Bert W. Strassburger Lipid Center (R.S.G., D.H., H.L., A.S.) and Department of Pathology (G.S., C.A.), and Thrombosis Unit (R.S.G., I.T., O.S.), Sheba Medical Center, Tel-Hashomer, Israel; Sackler Faculty of Medicine (R.S.G., D.H., G.S., H.L., C.A., I.T., O.S.), Tel-Aviv University, Tel-Aviv, Israel; and Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN (D.G.).
Camila AviviFrom the The Bert W. Strassburger Lipid Center (R.S.G., D.H., H.L., A.S.) and Department of Pathology (G.S., C.A.), and Thrombosis Unit (R.S.G., I.T., O.S.), Sheba Medical Center, Tel-Hashomer, Israel; Sackler Faculty of Medicine (R.S.G., D.H., G.S., H.L., C.A., I.T., O.S.), Tel-Aviv University, Tel-Aviv, Israel; and Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN (D.G.).
Ilia TamarinFrom the The Bert W. Strassburger Lipid Center (R.S.G., D.H., H.L., A.S.) and Department of Pathology (G.S., C.A.), and Thrombosis Unit (R.S.G., I.T., O.S.), Sheba Medical Center, Tel-Hashomer, Israel; Sackler Faculty of Medicine (R.S.G., D.H., G.S., H.L., C.A., I.T., O.S.), Tel-Aviv University, Tel-Aviv, Israel; and Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN (D.G.).
Aviv ShaishFrom the The Bert W. Strassburger Lipid Center (R.S.G., D.H., H.L., A.S.) and Department of Pathology (G.S., C.A.), and Thrombosis Unit (R.S.G., I.T., O.S.), Sheba Medical Center, Tel-Hashomer, Israel; Sackler Faculty of Medicine (R.S.G., D.H., G.S., H.L., C.A., I.T., O.S.), Tel-Aviv University, Tel-Aviv, Israel; and Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN (D.G.).
Ophira SalomonFrom the The Bert W. Strassburger Lipid Center (R.S.G., D.H., H.L., A.S.) and Department of Pathology (G.S., C.A.), and Thrombosis Unit (R.S.G., I.T., O.S.), Sheba Medical Center, Tel-Hashomer, Israel; Sackler Faculty of Medicine (R.S.G., D.H., G.S., H.L., C.A., I.T., O.S.), Tel-Aviv University, Tel-Aviv, Israel; and Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN (D.G.). ophiras@sheba.health.gov.il.
Tel Aviv University · IL

Funding

Physiology and Molecular Biology of Factor XIR01HL058837 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI GAILANI, DAVID · 1997 to 2017
$6.4M
Factor Xl in Vascular ThrombosisR01HL081326 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI GAILANI, DAVID · 2007 to 2017
$3.5M
NHLBI NIH HHS R01 HL058837NHLBI NIH HHS R01 HL081326
6 · The paper itself

Abstract

objectiveAtherosclerosis 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

resultsApolipoprotein 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.

conclusionsFXI deprivation was shown to slow down atherogenesis in mice. The results suggest that the development of atherosclerosis can be prevented by targeting FXI.

Indexed as

AnimalsAortaAortic DiseasesApolipoproteins EAtherosclerosisBiomarkersCholesterolDisease Models, AnimalFactor XIFactor XI DeficiencyGenetic Predisposition to DiseaseLipoproteins, LDLMacrophagesMaleMice, Inbred C57BLMice, KnockoutApolipoproteins EBiomarkersCholesterolFactor XILipoproteins, LDLatherosclerosisfactor XI

Identifiers

PMID26800563
PMCPMC4785893
OpenAlexW2286759685

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.