Evidence map›Paper›PMID 22982464›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Fibroblast growth factor-2 is required for vasa vasorum plexus stability in hypercholesterolemic mice.

Jessica I Mollmark, Andrew J-H Park, Justin Kim, Thomas Z Wang, Sarah Katzenell, Samantha L Shipman, Lyubomir G Zagorchev, Michael Simons, Mary Jo Mulligan-Kehoe

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. Promising Adventitia in Atherosclerosis.Current vascular pharmacology · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Association of FGF-2 Concentrations with Atheroma Progression in Chronic Kidney Disease Patients.Clinical journal of the American Society of Nephrology : CJASN · 2018
    Observational
  10. Article
  11. Review
  12. Integrin signaling in atherosclerosis.Cellular and molecular life sciences : CMLS · 2017
    Review
  13. Review
  14. Nox and Inflammation in the Vascular Adventitia.Hypertension (Dallas, Tex. : 1979) · 2016
    Review
  15. Vasa vasorum in atherosclerosis and clinical significance.International journal of molecular sciences · 2015
    Review
  16. Syndecan 4 is required for endothelial alignment in flow and atheroprotective signaling.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  17. Review
  18. Transforming growth factor-beta (TGF-β) in the pathogenesis of hereditary thoracic aneurysm disorders.Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Jessica I Mollmark *Departments of Surgery, Vascular Section (J.I.M., A.J.-H.P., J.K., T.Z.W., M.J.M.-K.), Immunology and Microbiology (S.K.), Medicine, Cardiology Section (S.L.S.), and Thayer School of Engineering (L.G.Z.), Dartmouth Medical School, Lebanon, NH; and Department of Internal Medicine, Cardiovascular Medicine Section, Yale University School of Medicine, New Haven, CT (M.S.).
Andrew J-H Park *Departments of Surgery, Vascular Section (J.I.M., A.J.-H.P., J.K., T.Z.W., M.J.M.-K.), Immunology and Microbiology (S.K.), Medicine, Cardiology Section (S.L.S.), and Thayer School of Engineering (L.G.Z.), Dartmouth Medical School, Lebanon, NH; and Department of Internal Medicine, Cardiovascular Medicine Section, Yale University School of Medicine, New Haven, CT (M.S.).
Justin KimDepartments of Surgery, Vascular Section (J.I.M., A.J.-H.P., J.K., T.Z.W., M.J.M.-K.), Immunology and Microbiology (S.K.), Medicine, Cardiology Section (S.L.S.), and Thayer School of Engineering (L.G.Z.), Dartmouth Medical School, Lebanon, NH; and Department of Internal Medicine, Cardiovascular Medicine Section, Yale University School of Medicine, New Haven, CT (M.S.).
Thomas Z WangDepartments of Surgery, Vascular Section (J.I.M., A.J.-H.P., J.K., T.Z.W., M.J.M.-K.), Immunology and Microbiology (S.K.), Medicine, Cardiology Section (S.L.S.), and Thayer School of Engineering (L.G.Z.), Dartmouth Medical School, Lebanon, NH; and Department of Internal Medicine, Cardiovascular Medicine Section, Yale University School of Medicine, New Haven, CT (M.S.).
Sarah KatzenellDepartments of Surgery, Vascular Section (J.I.M., A.J.-H.P., J.K., T.Z.W., M.J.M.-K.), Immunology and Microbiology (S.K.), Medicine, Cardiology Section (S.L.S.), and Thayer School of Engineering (L.G.Z.), Dartmouth Medical School, Lebanon, NH; and Department of Internal Medicine, Cardiovascular Medicine Section, Yale University School of Medicine, New Haven, CT (M.S.).
Samantha L ShipmanDepartments of Surgery, Vascular Section (J.I.M., A.J.-H.P., J.K., T.Z.W., M.J.M.-K.), Immunology and Microbiology (S.K.), Medicine, Cardiology Section (S.L.S.), and Thayer School of Engineering (L.G.Z.), Dartmouth Medical School, Lebanon, NH; and Department of Internal Medicine, Cardiovascular Medicine Section, Yale University School of Medicine, New Haven, CT (M.S.).
Lyubomir G ZagorchevDepartments of Surgery, Vascular Section (J.I.M., A.J.-H.P., J.K., T.Z.W., M.J.M.-K.), Immunology and Microbiology (S.K.), Medicine, Cardiology Section (S.L.S.), and Thayer School of Engineering (L.G.Z.), Dartmouth Medical School, Lebanon, NH; and Department of Internal Medicine, Cardiovascular Medicine Section, Yale University School of Medicine, New Haven, CT (M.S.).
Michael SimonsDepartments of Surgery, Vascular Section (J.I.M., A.J.-H.P., J.K., T.Z.W., M.J.M.-K.), Immunology and Microbiology (S.K.), Medicine, Cardiology Section (S.L.S.), and Thayer School of Engineering (L.G.Z.), Dartmouth Medical School, Lebanon, NH; and Department of Internal Medicine, Cardiovascular Medicine Section, Yale University School of Medicine, New Haven, CT (M.S.).
Mary Jo Mulligan-KehoeDepartments of Surgery, Vascular Section (J.I.M., A.J.-H.P., J.K., T.Z.W., M.J.M.-K.), Immunology and Microbiology (S.K.), Medicine, Cardiology Section (S.L.S.), and Thayer School of Engineering (L.G.Z.), Dartmouth Medical School, Lebanon, NH; and Department of Internal Medicine, Cardiovascular Medicine Section, Yale University School of Medicine, New Haven, CT (M.S.).
Dartmouth College · US

Funding

Translational Engineering in Cancer (TEC)P30CA023108 · NCI · DARTMOUTH COLLEGE · PI Steven D Leach · 1985 to 2026
$91.3M
Angiogensis and ischemiaR01HL053793 · NHLBI · YALE UNIVERSITY · PI SIMONS, MICHAEL · 1996 to 2017
$7.3M
Mechanisms of PAI-1 Induced Anti-AngiogenesisR01HL069948 · NHLBI · DARTMOUTH COLLEGE · PI MULLIGAN-KEHOE, MARY JO · 2003 to 2011
$2.6M
NCI NIH HHS P30 CA023108NHLBI NIH HHS HL53793NHLBI NIH HHS HL69948NHLBI NIH HHS R01 HL053793NHLBI NIH HHS R01 HL069948
6 · The paper itself

Abstract

objectiveVasa vasorum are angiogenic in advanced stages of human atherosclerosis and hypercholesterolemic mouse models. Fibroblast growth factor-2 (FGF-2) is the predominant angiogenic growth factor in the adventitia and plaque of hypercholesterolemic low-density lipoprotein receptor-deficient/apolipoprotein B(100/100) mice (DKO). FGF-2 seems to play a role in the formation of a distinct vasa vasorum network. This study examined the vasa vasorum structure and its relationship to FGF-2. METHODS AND

resultsDKO mice treated with saline, antiangiogenic recombinant plasminogen activator inhibitor-1(23) (rPAI-1(23)), or soluble FGF receptor 1 were perfused with fluorescein-labeled Lycopersicon esculentum lectin. Confocal images of FGF-2-probed descending aorta adventitia show that angiogenic vasa vasorum form a plexus-like network in saline-treated DKO similar to the FGF-2 pattern of distribution. Mice treated with rPAI-1(23) and soluble FGF receptor 1 lack a plexus; FGF-2 and vasa vasorum density and area are significantly reduced. A perlecan/FGF-2 complex is critical for plexus stability. Excess plasmin produced in rPAI-1(23)-treated DKO mice degrades perlecan and destabilizes the plexus. Plasmin activity and plaque size measured in DKO and DKO/plasminogen activator inhibitor-1(-)(/-) mice demonstrate that elevated plasmin activity contributes to reduced plaque size.

conclusionsAn FGF-2/perlecan complex is required for vasa vasorum plexus stability. Elevated plasmin activity plays a significant inhibitory role in vasa vasorum plexus and plaque development.

Indexed as

Neovascularization, PathologicAngiogenesis InhibitorsAnimalsAortaAortic DiseasesApolipoprotein B-100Apolipoproteins BAtherosclerosisCholesterol, DietaryDisease Models, AnimalFibrinolysinFibroblast Growth Factor 2Gene Transfer TechniquesHeparan Sulfate ProteoglycansHypercholesterolemiaMiceAngiogenesis InhibitorsApob protein, mouseApolipoprotein B-100Apolipoproteins BCholesterol, DietaryFibrinolysinFibroblast Growth Factor 2Heparan Sulfate ProteoglycansperlecanReceptor, Fibroblast Growth Factor, Type 1Receptors, LDL

Identifiers

PMID22982464
PMCPMC3819102
OpenAlexW2172038422

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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.