Evidence map›Paper›PMID 27006449›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016

Phenotypic transformation of intimal and adventitial lymphatics in atherosclerosis: a regulatory role for soluble VEGF receptor 2.

Mahdi Taher, Shintaro Nakao, Souska Zandi, Mark I Melhorn, K C Hayes, Ali Hafezi-Moghadam

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Promising Adventitia in Atherosclerosis.Current vascular pharmacology · 2025
    Review
  7. Article
  8. Article
  9. The Role of VEGF Family in Lipid Metabolism.Current pharmaceutical biotechnology · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. The CD44-HA axis and inflammation in atherosclerosis: A temporal perspective.Matrix biology : journal of the International Society for Matrix Biology · 2019
    Review
  19. Review
  20. Cardiac lymphatics in health and disease.Nature reviews. Cardiology · 2019
    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

6 authors at 5 institutions in 2 countries.

Mahdi TaherCenter for Excellence in Functional and Molecular Imaging, Brigham and Women's Hospital, Boston, Massachusetts, USA; Department of Radiology and Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, and Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA; Institute of Biochemistry, Charité University Medical Center, Berlin, Germany; and.
Shintaro NakaoCenter for Excellence in Functional and Molecular Imaging, Brigham and Women's Hospital, Boston, Massachusetts, USA; Department of Radiology and Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, and Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA;
Souska ZandiCenter for Excellence in Functional and Molecular Imaging, Brigham and Women's Hospital, Boston, Massachusetts, USA; Department of Radiology and Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, and Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA;
Mark I MelhornCenter for Excellence in Functional and Molecular Imaging, Brigham and Women's Hospital, Boston, Massachusetts, USA; Department of Radiology and Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, and Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA;
K C HayesDepartment of Biology, Brandeis University, Waltham, Massachusetts, USA.
Ali Hafezi-MoghadamCenter for Excellence in Functional and Molecular Imaging, Brigham and Women's Hospital, Boston, Massachusetts, USA; Department of Radiology and Angiogenesis Laboratory, Massachusetts Eye and Ear Infirmary, and Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA; ahm@bwh.harvard.edu.
Harvard University · USBrandeis University · USBrigham and Women's Hospital · USMassachusetts Eye and Ear Infirmary · USUniversity Medical Center · US

Funding

Non-Invasive Molecular Imaging in Early Diagnosis of Diabetic ComplicationsDP3DK108238 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI HAFEZI-MOGHADAM, ALI · 2015 to 2015
$1.7M
NIDDK NIH HHS DP3 DK108238
6 · The paper itself

Abstract

The role of lymphatics in atherosclerosis is not yet understood. Here, we investigate lymphatic growth dynamics and marker expression in atherosclerosis in apolipoprotein E-deficient (apoE(-/-)) mice. The prolymphangiogenic growth factor, VEGF-C, was elevated in atherosclerotic aortic walls. Despite increased VEGF-C, we found that adventitial lymphatics regress during the course of formation of atherosclerosis (P < 0.01). Similar to lymphatic regression, the number of lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1(+)) macrophages decreased in the aortic adventitia of apoE(-/-) mice with atherosclerosis (P < 0.01). Intimal lymphatics in the atherosclerotic lesions exhibited an atypical phenotype, with the expression of podoplanin and VEGF receptor 3 (VEGFR-3) but not of LYVE-1 and prospero homeobox protein 1. In the aortas of atherosclerotic animals, we found markedly increased soluble VEGFR-2. We hypothesized that the elevated soluble VEGFR-2 that was found in the aortas of apoE(-/-) mice with atherosclerosis binds to and diminishes the activity of VEGF-C. This trapping mechanism explains, despite increased VEGF-C in the atherosclerotic aortas, how adventitial lymphatics regress. Lymphatic regression impedes the drainage of lipids, growth factors, inflammatory cytokines, and immune cells. Insufficient lymphatic drainage could thus exacerbate atherosclerosis formation. Our study contributes new insights to previously unknown dynamic changes of adventitial lymphatics. Targeting soluble VEGFR-2 in atherosclerosis may provide a new strategy for the liberation of endogenous VEGF-C and the prevention of lymphatic regression.-Taher, M., Nakao, S., Zandi, S., Melhorn, M. I., Hayes, K. C., Hafezi-Moghadam, A. Phenotypic transformation of intimal and adventitial lymphatics in atherosclerosis: a regulatory role for soluble VEGF receptor 2.

Indexed as

AdventitiaCollagen Type VILymphangiogenesisAgingAnimalsApolipoproteins EAtherosclerosisGlycoproteinsMembrane GlycoproteinsMembrane Transport ProteinsMice, KnockoutPodoplaninVascular Endothelial Growth Factor Receptor-2Apolipoproteins ECollagen Type VIGlycoproteinsKdr protein, mouseLYVE1 protein, mouseMembrane GlycoproteinsMembrane Transport ProteinsPdpn protein, mousePodoplaninVascular Endothelial Growth Factor Receptor-2lymphangiogenesisLYVE-1macrophagespodoplaninVEGF-C

Identifiers

PMID27006449
PMCPMC4904291
OpenAlexW2303623770

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.