Evidence map›Paper›PMID 24864317›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2014

The road to rack and ruin: selecting deleterious mitochondrial DNA variants.

Ian J Holt, Dave Speijer, Thomas B L Kirkwood

Abstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. What cost mitochondria? The maintenance of functional mitochondrial DNA within and across generations.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Review
  7. Quality matters: how does mitochondrial network dynamics and quality control impact on mtDNA integrity?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    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

3 authors.

Ian J HoltMRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK iholt@nimr.mrc.ac.uk.
Dave SpeijerDepartment of Medical Biochemistry, Academic Medical Centre, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.
Thomas B L KirkwoodInstitute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne NE4 5PL, UK.

Funding

Biotechnology and Biological Sciences Research Council BB/C008200/1Biotechnology and Biological Sciences Research Council BB/F012802/1Medical Research Council MC_U105663140Medical Research Council MC_UP_1202/14Medical Research Council MR/K006312/1
6 · The paper itself

Abstract

Mitochondria constitute the major energy-producing compartment of the eukaryotic cell. These organelles contain many molecules of DNA that contribute only a handful of proteins required for energy production. Mutations in the DNA of mitochondria were identified as a cause of human disease a quarter of a century ago, and they have subsequently been implicated in ageing. The process whereby deleterious variants come to dominate a cell, tissue or human is the subject of debate. It is likely to involve multiple, often competing, factors, as selection pressures on mitochondrial DNA can be both indirect and intermittent, and are subjected to rapid change. Here, we assess the different models and the prospects for preventing the accumulation of deleterious mitochondrial DNA variants with time.

Indexed as

Genetic VariationSelection, GeneticAgingDNA, MitochondrialDNA ReplicationHumansMitochondriaMutationDNA, MitochondrialDNAmitochondriamutation

Identifiers

PMID24864317
PMCPMC4032523

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.