Evidence map›Paper›PMID 31154825›Full record

ArticleCirculation2019

Caveolin-1 Regulates Atherogenesis by Attenuating Low-Density Lipoprotein Transcytosis and Vascular Inflammation Independently of Endothelial Nitric Oxide Synthase Activation.

Cristina M Ramírez, Xinbo Zhang, Chirosree Bandyopadhyay, Noemi Rotllan, Michael G Sugiyama, Binod Aryal, Xinran Liu, Shun He, Jan R Kraehling, Victoria Ulrich and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Circulation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

93 citing papers in PubMed, 148 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Article
  6. Review
  7. Article
  8. Role of Caveolae and Caveolin in Vascular Physiology and Pathology.Journal of the American Heart Association · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Nitrosation of CD36 Regulates Endothelial Function and Serum Lipids.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
  18. Exploring the Associations of Maternal and NeonatalIndian journal of clinical biochemistry : IJCB · 2025
    Article
  19. Review
  20. Article

33 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

21 authors at 1 institution in 1 country.

Cristina M RamírezVascular Biology and Therapeutics Program (C.M.R., X.Z., N.R., B.A., J.R.K., V.U., Y.S., W.C.S., C.F.-H.), Yale University School of Medicine, New Haven, CT.
Xinbo ZhangVascular Biology and Therapeutics Program (C.M.R., X.Z., N.R., B.A., J.R.K., V.U., Y.S., W.C.S., C.F.-H.), Yale University School of Medicine, New Haven, CT.
Chirosree BandyopadhyayCardiovascular Research Center, Department of Internal Medicine and Cell Biology (C.B., M.A.S.), Yale University School of Medicine, New Haven, CT.
Noemi RotllanVascular Biology and Therapeutics Program (C.M.R., X.Z., N.R., B.A., J.R.K., V.U., Y.S., W.C.S., C.F.-H.), Yale University School of Medicine, New Haven, CT.
Michael G SugiyamaKeenan Research Centre and Departments of Laboratory Medicine and Pathobiology, Biochemistry and Medicine, University of Toronto, ON, Canada (M.G.S., W.L.L.).
Binod AryalVascular Biology and Therapeutics Program (C.M.R., X.Z., N.R., B.A., J.R.K., V.U., Y.S., W.C.S., C.F.-H.), Yale University School of Medicine, New Haven, CT.
Xinran LiuDepartment of Cell Biology (X.L.), Yale University School of Medicine, New Haven, CT.
Shun HeCenter for System Biology, Massachusetts General Hospital and Harvard Medical School, Boston (S.H., F.K.S.).
Jan R KraehlingVascular Biology and Therapeutics Program (C.M.R., X.Z., N.R., B.A., J.R.K., V.U., Y.S., W.C.S., C.F.-H.), Yale University School of Medicine, New Haven, CT.
Victoria UlrichVascular Biology and Therapeutics Program (C.M.R., X.Z., N.R., B.A., J.R.K., V.U., Y.S., W.C.S., C.F.-H.), Yale University School of Medicine, New Haven, CT.
Chin Sheng LinDivision of Cardiology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan (C.S.L.).
Heino VelazquezSection of Nephrology (H.V.), Yale University School of Medicine, New Haven, CT.
Miguel A LasunciónCardiovascular Research Center, Department of Internal Medicine and Cell Biology (C.B., M.A.S.), Yale University School of Medicine, New Haven, CT.
Guangxin LiDepartments of Cell Biology and Biomedical Engineering (G.L., G.T.), Yale University School of Medicine, New Haven, CT.
Yajaira SuárezVascular Biology and Therapeutics Program (C.M.R., X.Z., N.R., B.A., J.R.K., V.U., Y.S., W.C.S., C.F.-H.), Yale University School of Medicine, New Haven, CT.
George TellidesDepartments of Cell Biology and Biomedical Engineering (G.L., G.T.), Yale University School of Medicine, New Haven, CT.
Filip K SwirskiCenter for System Biology, Massachusetts General Hospital and Harvard Medical School, Boston (S.H., F.K.S.).
Warren L LeeKeenan Research Centre and Departments of Laboratory Medicine and Pathobiology, Biochemistry and Medicine, University of Toronto, ON, Canada (M.G.S., W.L.L.).
Martin A SchwartzDepartment of Cell Biology (M.A.S.), Yale University School of Medicine, New Haven, CT.
William C SessaVascular Biology and Therapeutics Program (C.M.R., X.Z., N.R., B.A., J.R.K., V.U., Y.S., W.C.S., C.F.-H.), Yale University School of Medicine, New Haven, CT.
Carlos Fernández-HernandoVascular Biology and Therapeutics Program (C.M.R., X.Z., N.R., B.A., J.R.K., V.U., Y.S., W.C.S., C.F.-H.), Yale University School of Medicine, New Haven, CT.
Yale University · US

Funding

Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Richard A Flavell · 1993 to 2026
$44.0M
Novel insights into the molecular and cellular mechanism regulating lipid metabolism and atherosclerosisR35HL135820 · NHLBI · YALE UNIVERSITY · PI FERNANDEZ HERNANDO, CARLOS · 2017 to 2023
$6.0M
Integrins in the Endothelial Response to Fluid Shear StressR01HL075092 · NHLBI · YALE UNIVERSITY · PI SCHWARTZ, MARTIN A · 2004 to 2019
$5.1M
microRNAs in vascular diseasesR01HL105945 · NHLBI · YALE UNIVERSITY · PI SUAREZ, YAJAIRA · 2011 to 2020
$3.7M
HL-Regulation of Angiogenesis in the Obese Adipose Tissue by Secreted microRNAsR01HL135012 · NHLBI · YALE UNIVERSITY · PI SUAREZ, YAJAIRA · 2017 to 2020
$2.1M
NHLBI NIH HHS R01 HL075092NHLBI NIH HHS R01 HL105945NHLBI NIH HHS R01 HL135012NHLBI NIH HHS R35 HL135820NIDDK NIH HHS P30 DK045735
6 · The paper itself

Abstract

backgroundAtherosclerosis is driven by synergistic interactions between pathological, biomechanical, inflammatory, and lipid metabolic factors. Our previous studies demonstrated that absence of caveolin-1 (Cav1)/caveolae in hyperlipidemic mice strongly inhibits atherosclerosis, which was attributed to activation of endothelial nitric oxide (NO) synthase (eNOS) and increased production of NO and reduced inflammation and low-density lipoprotein trafficking. However, the contribution of eNOS activation and NO production in the athero-protection of Cav1 and the exact mechanisms by which Cav1/caveolae control the pathogenesis of diet-induced atherosclerosis are still not clear.

methodsTriple-knockout mouse lacking expression of eNOS, Cav1, and Ldlr were generated to explore the role of NO production in Cav1-dependent athero-protective function. The effects of Cav1 on lipid trafficking, extracellular matrix remodeling, and vascular inflammation were studied both in vitro and in vivo with a mouse model of diet-induced atherosclerosis. The expression of Cav1 and distribution of caveolae regulated by flow were analyzed by immunofluorescence staining and transmission electron microscopy.

resultsWe found that absence of Cav1 significantly suppressed atherogenesis in Ldlr

conclusionsThese findings support a role for Cav1/caveolae as a central regulator of atherosclerosis that links biomechanical, metabolic, and inflammatory pathways independently of endothelial eNOS activation and NO production.

Indexed as

AnimalsAtherosclerosisCaveolin 1Cells, CulturedDogsEndothelium, VascularEnzyme ActivationFemaleHumansLipoproteins, LDLMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNitric Oxide Synthase Type IIICaveolin 1Lipoproteins, LDLNitric Oxide Synthase Type IIINos3 protein, mouseatherosclerosiscaveolaeextracellular matrixfibronectinsinflammationnitric oxide synthase type IIItranscytosis

Identifiers

PMID31154825
PMCPMC6778687
OpenAlexW2948668990

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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.