Evidence map›Paper›PMID 33430172›Full record

ArticleBiomolecules2021

The Presence of Cholesteryl Ester Transfer Protein (CETP) in Endothelial Cells Generates Vascular Oxidative Stress and Endothelial Dysfunction.

Amarylis C B A Wanschel, Daniele M Guizoni, Estela Lorza-Gil, Alessandro G Salerno, Adriene A Paiva, Gabriel G Dorighello, Ana Paula Davel, Wayne Balkan, Joshua M Hare, Helena C F Oliveira

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2021. 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
1.8field-weighted citation impact, top 15% 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, 28 citations in OpenAlex.

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  8. Association ofInternational journal of molecular sciences · 2024
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  15. Association ofInternational journal of molecular sciences · 2023
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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

10 authors at 2 institutions in 2 countries.

Amarylis C B A WanschelDepartment of Structural and Functional Biology, Institute of Biology, State University of Campinas, Campinas 13083-970, Brazil.ORCID 0000-0002-5603-7983
Daniele M GuizoniDepartment of Structural and Functional Biology, Institute of Biology, State University of Campinas, Campinas 13083-970, Brazil.ORCID 0000-0001-7317-6371
Estela Lorza-GilDepartment of Structural and Functional Biology, Institute of Biology, State University of Campinas, Campinas 13083-970, Brazil.
Alessandro G SalernoDepartment of Structural and Functional Biology, Institute of Biology, State University of Campinas, Campinas 13083-970, Brazil.ORCID 0000-0002-7688-5904
Adriene A PaivaDepartment of Structural and Functional Biology, Institute of Biology, State University of Campinas, Campinas 13083-970, Brazil.
Gabriel G DorighelloDepartment of Structural and Functional Biology, Institute of Biology, State University of Campinas, Campinas 13083-970, Brazil.ORCID 0000-0001-6566-4244
Ana Paula DavelDepartment of Structural and Functional Biology, Institute of Biology, State University of Campinas, Campinas 13083-970, Brazil.ORCID 0000-0002-9862-4262
Wayne BalkanInterdisciplinary Stem Cell Institute, Miller School of Medicine, University of Miami, Miami, FL 33146, USA.ORCID 0000-0003-0405-0489
Joshua M HareInterdisciplinary Stem Cell Institute, Miller School of Medicine, University of Miami, Miami, FL 33146, USA.ORCID 0000-0002-7751-5032
Helena C F OliveiraDepartment of Structural and Functional Biology, Institute of Biology, State University of Campinas, Campinas 13083-970, Brazil.ORCID 0000-0003-0119-6992
Universidade Estadual de Campinas (UNICAMP) · BRUniversity of Miami · US

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo (Fapesp) 13/09347-3
6 · The paper itself

Abstract

Endothelial dysfunction precedes atherosclerosis and is an independent predictor of cardiovascular events. Cholesterol levels and oxidative stress are key contributors to endothelial damage, whereas high levels of plasma high-density lipoproteins (HDL) could prevent it. Cholesteryl ester transfer protein (CETP) is one of the most potent endogenous negative regulators of HDL-cholesterol. However, whether and to what degree CETP expression impacts endothelial function, and the molecular mechanisms underlying the vascular effects of CETP on endothelial cells, have not been addressed. Acetylcholine-induced endothelium-dependent relaxation of aortic rings was impaired in human CETP-expressing transgenic mice, compared to their non-transgenic littermates. However, endothelial nitric oxide synthase (eNOS) activation was enhanced. The generation of superoxide and hydrogen peroxide was increased in aortas from CETP transgenic mice, while silencing CETP in cultured human aortic endothelial cells effectively decreased oxidative stress promoted by all major sources of ROS: mitochondria and NOX2. The endoplasmic reticulum stress markers, known as GADD153, PERK, and ARF6, and unfolded protein response effectors, were also diminished. Silencing CETP reduced endothelial tumor necrosis factor (TNF) α levels, intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) expression, diminishing monocyte adhesion. These results support the notion that CETP expression negatively impacts endothelial cell function, revealing a new mechanism that might contribute to atherosclerosis.

Indexed as

Oxidative StressAnimalsCaveolinsCell Adhesion MoleculesCholesterol Ester Transfer ProteinsEndoplasmic Reticulum StressEndothelial CellsEndothelium, VascularEnzyme ActivationHumansMice, TransgenicNADPH OxidasesNitric Oxide Synthase Type IIIPhosphorylationReactive Oxygen SpeciesRNA, MessengerCaveolinsCell Adhesion MoleculesCholesterol Ester Transfer ProteinsNADPH OxidasesNitric Oxide Synthase Type IIIReactive Oxygen SpeciesRNA, MessengerCETPendoplasmic reticulum stressendothelial dysfunctionhydrogen peroxideIcam-1mitochondriamonocytesoxidative stresssuperoxideVcam-1

Identifiers

PMID33430172
PMCPMC7825632
OpenAlexW3118848356

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.