Evidence map›Paper›PMID 28169948›Full record

ArticleCurrent opinion in cardiology2017

Mitochondrial DNA mutations and cardiovascular disease.

Alexander W Bray, Scott W Ballinger

Open access · greenAbstract read
In one paragraph

Article in Current opinion in cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

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  8. Mitochondrial non-energetic function and embryonic cardiac development.Frontiers in cell and developmental biology · 2024
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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 1 institution in 1 country.

Alexander W BrayDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama, Birmingham, Alabama, USA.
Scott W Ballinger
University of Alabama at Birmingham · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
Sex hormones and arthritis in a long lived animal modelP30AG050886 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DAVID B ALLISON · 2015 to 2026
$11.3M
Training Program in Cardiovascular PathophysiologyT32HL007918 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BALLINGER, SCOTT W. · 1999 to 2018
$3.6M
Mitochondrial Nuclear Interactions and CVD SusceptibilityR01HL103859 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BALLINGER, SCOTT W. · 2011 to 2014
$2.1M
Mitochondrial Genetic Background Influences Susceptibility to AtherosclerosisF30HL127992 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRAY, ALEXANDER WENDELL · 2015 to 2016
$76k
NHLBI NIH HHS F30 HL127992NHLBI NIH HHS R01 HL103859NHLBI NIH HHS T32 HL007918NIA NIH HHS P30 AG050886NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

purpose of reviewCardiovascular disease (CVD) is responsible for more morbidity and mortality worldwide than any other ailment. Strategies for reducing CVD prevalence must involve identification of individuals at high risk for these diseases, and the prevention of its initial development. Such preventive efforts are currently limited by an incomplete understanding of the genetic determinants of CVD risk. In this review, evidence for the involvement of inherited mitochondrial mutations in development of CVD is examined. RECENT

findingsSeveral forms of CVD have been documented in the presence of pathogenic mitochondrial DNA (mtDNA) mutations, both in isolation and as part of larger syndromes. Other 'natural' mtDNA polymorphisms not overtly tied to any pathology have also been associated with alterations in mitochondrial function and individual risk for CVD, but until very recently these studies have been merely correlative. Fortunately, novel animal models are now allowing investigators to define a causal relationship between inherited 'natural' mtDNA polymorphisms, and cardiovascular function and pathology. SUMMARY: Cardiovascular involvement is highly prevalent among patients with pathogenic mtDNA mutations. The relationship between CVD susceptibility and 'natural' mtDNA polymorphisms requires further investigation, but will be aided in the near future by several novel experimental models.

Identifiers

PMID28169948
PMCPMC5608632
OpenAlexW2588180015

What OpenQuestion holds

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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.