Evidence map›Paper›PMID 21384259›Full record

ReviewCurrent atherosclerosis reports2011

Atherosclerosis: an epigenetic balancing act that goes wrong.

Gertrud Lund, Silvio Zaina

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current atherosclerosis reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 42 citations in OpenAlex.

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  12. Epigenetics across the human lifespan.Frontiers in cell and developmental biology · 2014
    Review
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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

2 authors at 2 institutions in 1 country.

Gertrud LundDepartment of Genetic Engineering, CINVESTAV, Unidad Irapuato, Km 9.6 Libramiento Norte Carretera Irapuato-León, 36500 Irapuato, Mexico. glund@ira.cinvestav.mx
Silvio Zaina
Center for Research and Advanced Studies of the National Polytechnic Institute · MXUniversidad de Guanajuato · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence points to dietary lipids and their derivates as dynamic modulators of pro- or anti-inflammatory gene expression pathways via their ability to interact with nuclear receptors that are central to the regulation of numerous biological functions, including lipid metabolism, inflammatory mediator production, and vascular homeostasis. The biological effects of these receptors are the result of a finely tuned equilibrium between gene activation and repression, resulting from their ability to switch between chromatin-remodelling co-repressor and co-activator partners. The aim of this review is to discuss the concept that selected dietary components induce an atherosclerotic cellular phenotype, at least in part, by imposing epigenetic marks that shift the physiologic program of differential gene activation and repression. Aberrant epigenetic marks are seeded in promoter sequences as well as in intragenic sequences where they might regulate transcript splicing.

Indexed as

AtherosclerosisEpigenomicsGene Expression RegulationAnimalsDietary FatsDiet, AtherogenicDNA MethylationEnvironmental ExposureGene SilencingHomeostasisHumansInflammation MediatorsLife StyleLipid MetabolismModels, BiologicalPhenotypeDietary FatsInflammation MediatorsReceptors, Cytoplasmic and Nuclear

Identifiers

PMID21384259
OpenAlexW2106551804

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.