Evidence map›Paper›PMID 30671084›Full record

ArticleFrontiers in genetics2018

New mtDNA Association Model, MutPred Variant Load, Suggests Individuals With Multiple Mildly Deleterious mtDNA Variants Are More Likely to Suffer From Atherosclerosis.

Agnieszka Piotrowska-Nowak, Joanna L Elson, Agnieszka Sobczyk-Kopciol, Aleksandra Piwonska, Aleksandra Puch-Walczak, Wojciech Drygas, Rafal Ploski, Ewa Bartnik, Katarzyna Tonska

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Mitochondrial Genome Variation in Polish Elite Athletes.International journal of molecular sciences · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. To Be a Champion of the 24-h Ultramarathon Race. If Not the Heart ... Mosaic Theory?International journal of environmental research and public health · 2021
    Article
  11. Article
  12. Review
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 6 institutions in 3 countries.

Agnieszka Piotrowska-NowakFaculty of Biology, Institute of Genetics and Biotechnology, University of Warsaw, Warsaw, Poland.
Joanna L ElsonInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.
Agnieszka Sobczyk-KopciolDepartment of General Biology and Parasitology, Medical University of Warsaw, Warsaw, Poland.
Aleksandra PiwonskaDepartment of Epidemiology, Cardiovascular Disease Prevention and Health Promotion, Institute of Cardiology, Warsaw, Poland.
Aleksandra Puch-WalczakDepartment of Prevention and Education, Department of Arterial Hypertension and Diabetology, Medical University of Gdansk, Gdansk, Poland.
Wojciech DrygasDepartment of Epidemiology, Cardiovascular Disease Prevention and Health Promotion, Institute of Cardiology, Warsaw, Poland.
Rafal PloskiDepartment of Medical Genetics, Medical University of Warsaw, Warsaw, Poland.
Ewa BartnikFaculty of Biology, Institute of Genetics and Biotechnology, University of Warsaw, Warsaw, Poland.
Katarzyna TonskaFaculty of Biology, Institute of Genetics and Biotechnology, University of Warsaw, Warsaw, Poland.
Institute of Cardiology · PLMedical University of Warsaw · PLUniversity of Warsaw · PLGdańsk Medical University · PLInstitute of Biochemistry and Biophysics, Polish Academy of Sciences · PLNewcastle University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The etiology of common complex diseases is multifactorial, involving both genetic, and environmental factors. A role for mitochondrial dysfunction and mitochondrial DNA (mtDNA) variation has been suggested in the pathogenesis of common complex traits. The aim of this study was to investigate a potential role of mtDNA variants in the development of obesity, diabetes, and atherosclerosis in the Polish population. Whole mtDNA sequences from 415 Polish individuals representing three disease cohorts and a control group were obtained using high-throughput sequencing. Two approaches for the assessment of mtDNA variation were applied, traditional mitochondrial haplogroup association analysis and the mutational or variant load model using the MutPred pathogenicity prediction algorithm for amino acid substitutions in humans. We present a possible association between mildly deleterious mtDNA variant load and atherosclerosis that might be due to having more than one likely mildly deleterious non-synonymous substitution. Moreover, it seems largely dependent upon a few common haplogroup associated variants with MutPred score above 0.5.

Indexed as

atherosclerosiscommon complex diseasesmtDNA variationMutPredvariant load

Identifiers

PMID30671084
PMCPMC6332467
OpenAlexW2904691954

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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.