Evidence map›Paper›PMID 33436758›Full record

ArticleScientific reports2021

Examining the effect of mitochondrial DNA variants on blood pressure in two Finnish cohorts.

Jaakko Laaksonen, Pashupati P Mishra, Ilkka Seppälä, Leo-Pekka Lyytikäinen, Emma Raitoharju, Nina Mononen, Maija Lepistö, Henrikki Almusa, Pekka Ellonen, Nina Hutri-Kähönen and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. 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

15 authors at 5 institutions in 2 countries.

Jaakko LaaksonenDepartment of Clinical Chemistry, Fimlab Laboratories and Finnish Cardiovascular Research Center Tampere, Faculty of Medicine and Health Technology, Tampere University, Arvo Ylpön katu 34, PO Box 100, 33014, Tampere, Finland. jaakko.h.laaksonen@tuni.fi.ORCID 0000-0003-3577-6928
Pashupati P MishraDepartment of Clinical Chemistry, Fimlab Laboratories and Finnish Cardiovascular Research Center Tampere, Faculty of Medicine and Health Technology, Tampere University, Arvo Ylpön katu 34, PO Box 100, 33014, Tampere, Finland.
Ilkka SeppäläDepartment of Clinical Chemistry, Fimlab Laboratories and Finnish Cardiovascular Research Center Tampere, Faculty of Medicine and Health Technology, Tampere University, Arvo Ylpön katu 34, PO Box 100, 33014, Tampere, Finland.
Leo-Pekka LyytikäinenDepartment of Clinical Chemistry, Fimlab Laboratories and Finnish Cardiovascular Research Center Tampere, Faculty of Medicine and Health Technology, Tampere University, Arvo Ylpön katu 34, PO Box 100, 33014, Tampere, Finland.
Emma RaitoharjuDepartment of Clinical Chemistry, Fimlab Laboratories and Finnish Cardiovascular Research Center Tampere, Faculty of Medicine and Health Technology, Tampere University, Arvo Ylpön katu 34, PO Box 100, 33014, Tampere, Finland.
Nina MononenDepartment of Clinical Chemistry, Fimlab Laboratories and Finnish Cardiovascular Research Center Tampere, Faculty of Medicine and Health Technology, Tampere University, Arvo Ylpön katu 34, PO Box 100, 33014, Tampere, Finland.
Maija LepistöInstitute for Molecular Medicine (FIMM), University of Helsinki, Helsinki, Finland.
Henrikki AlmusaInstitute for Molecular Medicine (FIMM), University of Helsinki, Helsinki, Finland.
Pekka EllonenInstitute for Molecular Medicine (FIMM), University of Helsinki, Helsinki, Finland.
Nina Hutri-KähönenDepartment of Paediatrics, Tampere University Hospital and Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Markus JuonalaDepartment of Medicine, University of Turku, Turku, Finland.
Olli RaitakariCentre for Population Health Research, University of Turku and Turku University Hospital, Turku, Finland.
Mika KähönenDepartment of Clinical Physiology, Tampere University Hospital and Finnish Cardiovascular Research Center Tampere, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Jukka T SalonenDepartment of Public Health, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Terho LehtimäkiDepartment of Clinical Chemistry, Fimlab Laboratories and Finnish Cardiovascular Research Center Tampere, Faculty of Medicine and Health Technology, Tampere University, Arvo Ylpön katu 34, PO Box 100, 33014, Tampere, Finland.
Tampere University · FIUniversity of Helsinki · FITampere University Hospital · FIUniversity of Turku · FITampere University of Applied Sciences · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High blood pressure (BP) is a major risk factor for many noncommunicable diseases. The effect of mitochondrial DNA single-nucleotide polymorphisms (mtSNPs) on BP is less known than that of nuclear SNPs. We investigated the mitochondrial genetic determinants of systolic, diastolic, and mean arterial BP. MtSNPs were determined from peripheral blood by sequencing or with genome-wide association study SNP arrays in two independent Finnish cohorts, the Young Finns Study and the Finnish Cardiovascular Study, respectively. In total, over 4200 individuals were included. The effects of individual common mtSNPs, with an additional focus on sex-specificity, and aggregates of rare mtSNPs grouped by mitochondrial genes were evaluated by meta-analysis of linear regression and a sequence kernel association test, respectively. We accounted for the predicted pathogenicity of the rare variants within protein-encoding and the tRNA regions. In the meta-analysis of 87 common mtSNPs, we did not observe significant associations with any of the BP traits. Sex-specific and rare-variant analyses did not pinpoint any significant associations either. Our results are in agreement with several previous studies suggesting that mtDNA variation does not have a significant role in the regulation of BP. Future studies might need to reconsider the mechanisms thought to link mtDNA with hypertension.

Indexed as

Genome, MitochondrialPolymorphism, Single NucleotideAdultBlood PressureCohort StudiesDNA, MitochondrialFemaleFinlandGenome-Wide Association StudyGenotypeHumansHypertensionMaleMiddle AgedMitochondriaPhenotypeDNA, Mitochondrial

Identifiers

PMID33436758
PMCPMC7804469
OpenAlexW3119026980

What Socratic holds

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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 Socratic graph.