Evidence map›Paper›PMID 19583953›Full record

ArticleCell metabolism2009

Genetic evidence supporting a critical role of endothelial caveolin-1 during the progression of atherosclerosis.

Carlos Fernández-Hernando, Jun Yu, Yajaira Suárez, Christoph Rahner, Alberto Dávalos, Miguel A Lasunción, William C Sessa

Abstract read
In one paragraph

Article in Cell metabolism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
4.5field-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

121 citing papers in PubMed, 184 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Nitrosation of CD36 Regulates Endothelial Function and Serum Lipids.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
  8. Review
  9. Review
  10. Transcytosis of LDL Across Arterial Endothelium: Mechanisms and Therapeutic Targets.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  11. Caveolae: Metabolic Platforms at the Crossroads of Health and Disease.International journal of molecular sciences · 2025
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

61 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 2 countries.

Carlos Fernández-HernandoDepartment of Pharmacology, Yale University School of Medicine, New Haven, CT 06510, USA.
Jun Yu
Yajaira Suárez
Christoph Rahner
Alberto Dávalos
Miguel A Lasunción
William C Sessa
Yale University · USHospital Universitario Ramón y Cajal · ES

Funding

SOCS-1 and endothelial dysfunction in graft arteriosclerosisP01HL070295 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2001 to 2010
$17.9M
PHOSPHORYLATION AND ENDOTHELIAL NITRIC OXIDE PRODUCTIONR01HL064793 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2000 to 2016
$6.3M
Endothelial NOS by protein to protein interactionsR37HL061371 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2009 to 2017
$4.1M
Regulation of vascular remodeling &angiogenesis by NogoR01HL081190 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2005 to 2014
$4.1M
Endothelial NOS by Protein-Protein IntractionsR01HL061371 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 1999 to 2008
$3.6M
microRNA regulation of endothelial functionsR01HL096670 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2010 to 2013
$1.8M
Vascular Remodeling: Role of Nitric OxideR01HL057665 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C. · 1996 to 2004
$1.5M
NHLBI PROTEOMICS INITIATIVE-N01HV28186N01HV028186 · HV · YALE UNIVERSITY · PI WILLIAMS, KENNETH · 2002 to 2006
–
NHLBI NIH HHS N01 HV028186NHLBI NIH HHS N01-HV-28186NHLBI NIH HHS P01 HL070295NHLBI NIH HHS P01 HL70295NHLBI NIH HHS R01 HL057665NHLBI NIH HHS R01 HL061371NHLBI NIH HHS R01 HL064793NHLBI NIH HHS R01 HL081190NHLBI NIH HHS R01 HL096670NHLBI NIH HHS R01 HL57665NHLBI NIH HHS R01 HL61371NHLBI NIH HHS R01 HL64793NHLBI NIH HHS R37 HL061371
6 · The paper itself

Abstract

The accumulation of LDL-derived cholesterol in the artery wall is the initiating event that causes atherosclerosis. However, the mechanisms that lead to the initiation of atherosclerosis are still poorly understood. Here, by using endothelial cell-specific transgenesis of the caveolin-1 (Cav-1) gene in mice, we show the critical role of Cav-1 in promoting atherogenesis. Mice were generated lacking Cav-1 and apoE but expressing endothelial-specific Cav-1 in the double knockout background. Genetic ablation of Cav-1 on an apoE knockout background inhibits the progression of atherosclerosis, while re-expression of Cav-1 in the endothelium promotes lesion expansion. Mechanistically, the loss of Cav-1 reduces LDL infiltration into the artery wall, promotes nitric oxide production, and reduces the expression of leukocyte adhesion molecules, effects completely reversed in transgenic mice. In summary, this unique model provides physiological evidence supporting the important role of endothelial Cav-1 expression in regulating the entry of LDL into the vessel wall and the initiation of atherosclerosis.

Indexed as

AnimalsApolipoproteins EAtherosclerosisCaveolin 1Cholesterol, LDLDisease ProgressionEndothelium, VascularMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNitric OxideApolipoproteins ECaveolin 1Cholesterol, LDLNitric Oxide

Identifiers

PMID19583953
PMCPMC2735117
OpenAlexW2073331228

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.