Evidence map›Paper›PMID 23056349›Full record

ArticlePloS one2012

Mutation C3256T of mitochondrial genome in white blood cells: novel genetic marker of atherosclerosis and coronary heart disease.

Igor A Sobenin, Margarita A Sazonova, Maria M Ivanova, Andrey V Zhelankin, Veronika A Myasoedova, Anton Y Postnov, Serik D Nurbaev, Yuri V Bobryshev, Alexander N Orekhov

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

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  8. Detecting Rare Variants and Heteroplasmy of Mitochondrial DNA from High-Throughput Sequencing in Patients with Coronary Artery Disease.Medical science monitor : international medical journal of experimental and clinical research · 2020
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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

9 authors at 3 institutions in 2 countries.

Igor A SobeninLaboratory of Medical Genetics, Russian Cardiology Research and Production Complex, Russian Ministry of Health and Social Care, Moscow, Russian Federation.
Margarita A Sazonova
Maria M Ivanova
Andrey V Zhelankin
Veronika A Myasoedova
Anton Y Postnov
Serik D Nurbaev
Yuri V Bobryshev
Alexander N Orekhov
Research Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUInstitute for Atherosclerosis Research · RUMinistry of Health of the Russian Federation · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study was undertaken to examine the association between the level of heteroplasmy for the mutation C3256T in human white blood cells and the extent of carotid atherosclerosis, as well as the presence of coronary heart disease (CHD), the major clinical manifestation of atherosclerosis. Totally, 191 participants (84 men, 107 women) aged 65.0 years (SD 9.4) were recruited in the study; 45 (24%) of them had CHD. High-resolution B-mode ultrasonography of carotids was used to estimate the extent of carotid atherosclerosis by measuring of the carotid intima-media thickness (cIMT). DNA samples were obtained from whole venous blood, and then PCR and pyrosequencing were carried out. On the basis of pyrosequencing data, the levels of C3256T heteroplasmy in DNA samples were calculated. The presence of the mutant allele was detected in all study participants; the level of C3256T heteroplasmy in white blood cells ranged from 5% to 74%. The highly significant relationship between C3256T heteroplasmy level and predisposition to atherosclerosis was revealed. In individuals with low predisposition to atherosclerosis the mean level of C3256T heteroplasmy was 16.8%, as compared to 23.8% in moderately predisposed subjects, and further to 25.2% and 28.3% in significantly and highly predisposed subjects, respectively. The level of C3256T heteroplasmy of mitochondrial genome in human white blood cells is a biomarker of mitochondrial dysfunction and risk factor for atherosclerosis; therefore, it can be used as an informative marker of genetic susceptibility to atherosclerosis, coronary heart disease and myocardial infarction.

Indexed as

Genome, MitochondrialMutationAgedAtherosclerosisCoronary Artery DiseaseFemaleGenetic MarkersHumansLeukocytesMaleMiddle AgedGenetic Markers

Identifiers

PMID23056349
PMCPMC3462756
OpenAlexW2070259803

What OpenQuestion holds

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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.