Evidence map›Paper›PMID 25360389›Full record

ArticleAmerican journal of cardiovascular disease2014

Vascular hypercontractility and endothelial dysfunction before development of atherosclerosis in moderate dyslipidemia: role for nitric oxide and interleukin-6.

Vanessa Cavieres, Karla Valdes, Brayan Moreno, Rodrigo Moore-Carrasco, Daniel R Gonzalez

Open access · greenAbstract read
In one paragraph

Article in American journal of cardiovascular disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-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

20 citing papers in PubMed, 37 citations in OpenAlex.

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  19. Protective effects of heparin on endothelial cells in sepsis.International journal of clinical and experimental medicine · 2015
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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

5 authors at 1 institution in 1 country.

Vanessa CavieresDepartamento de Ciencias Basicas Biomedicas, Facultad de Ciencias de la Salud, Universidad de Talca Talca, Chile.
Karla ValdesDepartamento de Ciencias Basicas Biomedicas, Facultad de Ciencias de la Salud, Universidad de Talca Talca, Chile.
Brayan MorenoDepartamento de Ciencias Basicas Biomedicas, Facultad de Ciencias de la Salud, Universidad de Talca Talca, Chile.
Rodrigo Moore-CarrascoDepartamento de Bioquímica Clínica e Inmunohematologia, Facultad de Ciencias de la Salud, Universidad de Talca Talca, Chile ; Interdisciplinary Excellence Research Program on Healthy Aging (PIEI-ES), Universidad de Talca Talca 3460000, Chile.
Daniel R GonzalezDepartamento de Ciencias Basicas Biomedicas, Facultad de Ciencias de la Salud, Universidad de Talca Talca, Chile ; Interdisciplinary Excellence Research Program on Healthy Aging (PIEI-ES), Universidad de Talca Talca 3460000, Chile.
University of Talca · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a chronic disease that affects peripheral arteries and the aorta. Several inflammatory processes are required until the production of an atheroma. Before the atheroma appears, endothelial dysfunction is a key event. We hypothesized that endothelial dysfunction occurs in a mouse model of mild dyslipidemia, the mouse deficient in apolipoprotein E (apoE(+/-)). Using aortic rings preparation, we found that apoE(+/-) mice showed increased developed tension in response to KCl 60 mM when using a range a pre-loads from 0.5 to 2.0 grams (p = 0.038). Next, we tested the vasorelaxant capacity of apoE(+/-) aortas (pre-contracted with phenylephrine) in response to acetylcholine, an endothelium-dependent vasodilator. ApoE(+/-) aortas showed diminished vasorelaxation in a range of Ach concentrations (p = 0.0032). Next we assessed the levels of plasma NO metabolites, nitrite plus nitrate. These were significantly reduced, along with a significant decrease of the endothelial nitric oxide synthase in ApoE(+/-) mice. When we analyzed the morphology of the aortas in apoE(+/-) mice, these showed no signs of atheroma. In addition, we analyzed the levels of inflammatory cytokines, TNF-alpha, MCP-1 and interleukin 6 (Il-6). While TNF-alpha was similar in both groups, (18.3 ± 2 pg/mL in wild type vs. 17.5 ± 2 pg/mL in apoE(+/-)), MCP-1 was increased in ApoE deficient mice (71.5 ± 0.8 pg/mL in wild type vs. 85.1 ± 7.4 pg/mL in ApoE(+/-) mice, p = 0.006), along with IL-6 (24.7 ± 1.7 pg/ml in wild type vs. 47.1 ± 12.5 in ApoE mice, p = 0.0055). These results suggest that mild dyslipidemia produces a pro-inflammatory state, associated with diminished NOS and NO production, which produces endothelial dysfunction.

Indexed as

apoEAtherosclerosisendothelial dysfunctioneNOSnitric oxide

Identifiers

PMID25360389
PMCPMC4212886
OpenAlexW2145230277

What OpenQuestion holds

Textmetadata
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.