Evidence map›Paper›PMID 27358026›Full record

ReviewClinical science (London, England : 1979)2016

Mitochondrial health, the epigenome and healthspan.

Miguel A Aon, Sonia Cortassa, Magdalena Juhaszova, Steven J Sollott

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical science (London, England : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Optimized Nutrition in Mitochondrial Disease Correlates to Improved Muscle Fatigue, Strength, and Quality of Life.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  12. Review
  13. Epigenetics and Pregnancy: Conditional Snapshot or Rolling Event.International journal of molecular sciences · 2022
    Review
  14. Review
  15. Review
  16. Maternal Inflammation During Pregnancy and Offspring Brain Development: The Role of Mitochondria.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. Article
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

4 authors at 1 institution in 1 country.

Miguel A AonLaboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, U.S.A. miguel.aon@nih.gov.
Sonia CortassaLaboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, U.S.A.
Magdalena JuhaszovaLaboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, U.S.A.
Steven J SollottLaboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, U.S.A.
Institute on Aging · US

Funding

Control Mechanisms for Matching ATP Supply and Demand in Heart MitochondriaZIAAG000250 · NIA · NATIONAL INSTITUTE ON AGING · PI SOLLOTT, STEVEN · 2009 to 2024
$21.0M
GSK3b mediates convergence of protection signaling to limit mitochondrial damage ZIAAG000823 · NIA · NATIONAL INSTITUTE ON AGING · PI SOLLOTT, STEVEN · 2009 to 2016
$6.8M
Intramural NIH HHS Z99 AG999999
6 · The paper itself

Abstract

Food nutrients and metabolic supply-demand dynamics constitute environmental factors that interact with our genome influencing health and disease states. These gene-environment interactions converge at the metabolic-epigenome-genome axis to regulate gene expression and phenotypic outcomes. Mounting evidence indicates that nutrients and lifestyle strongly influence genome-metabolic functional interactions determining disease via altered epigenetic regulation. The mitochondrial network is a central player of the metabolic-epigenome-genome axis, regulating the level of key metabolites [NAD(+), AcCoA (acetyl CoA), ATP] acting as substrates/cofactors for acetyl transferases, kinases (e.g. protein kinase A) and deacetylases (e.g. sirtuins, SIRTs). The chromatin, an assembly of DNA and nucleoproteins, regulates the transcriptional process, acting at the epigenomic interface between metabolism and the genome. Within this framework, we review existing evidence showing that preservation of mitochondrial network function is directly involved in decreasing the rate of damage accumulation thus slowing aging and improving healthspan.

Indexed as

Energy MetabolismEpigenesis, GeneticGenome, HumanHealth StatusAdolescentAdultAgedAged, 80 and overAge FactorsAgingAnimalsChildChild, PreschoolDNA, MitochondrialGene-Environment InteractionGene Expression RegulationDNA, Mitochondrialacetylationadipose tissueagingautophagybiogenesiscaloric restrictioncardiovascular diseasechromatindietepigenetic modificationepigeneticshistonesmitochondriamitochondrial fusion–fissionmitophagy

Identifiers

PMID27358026
PMCPMC5066813
OpenAlexW2466333622

What OpenQuestion holds

Textmetadata
LicenceTDM
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.