Evidence map›Paper›PMID 33271282›Full record

ReviewFree radical biology & medicine2021

Mitochondria signaling to the epigenome: A novel role for an old organelle.

Janine Hertzog Santos

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 8% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

Janine Hertzog SantosNational Toxicology Program Laboratory (NTPL), National Toxicology Program (NTP), National Institute of Environmental Health Sciences (NIEHS), Research Triangle Park (RTP), NC, USA. Electronic address: janine.santos@nih.gov.
National Institute of Environmental Health Sciences · US

Funding

Gene Expression and MicroarraysZICES102445 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI GERRISH, KEVIN · 2009 to 2025
$31.6M
Intramural NIH HHS Z99 ES999999
6 · The paper itself

Abstract

Epigenetic modifications influence gene expression programs ultimately dictating physiological outcomes. In the past decades, an increasing body of work has demonstrated that the enzymes that deposit and/or remove epigenetic marks on DNA or histones use metabolites as substrates or co-factors, rendering the epigenome sensitive to metabolic changes. In this context, acetyl-CoA and α-ketoglutarate have been recognized as critical for epigenetics, impinging on histone marks and nuclear DNA methylation patterns. Given that these metabolites are primarily generated in the mitochondria through the tricarboxylic acid cycle (TCA), the requirement of proper mitochondrial function for maintenance of the epigenetic landscape seems obvious. Nevertheless, it was not until recently when the epigenomic outcomes of mitochondrial dysfunction were tested, revealing mitochondria's far-reaching impact on epigenetics. This review will focus on data that directly tested the role of mitochondria on the epigenetic landscape, the mechanisms by which mitochondrial dysfunction may dysregulate the epigenome and gene expression, and their potential implications to health and disease.

Indexed as

Epigenesis, GeneticEpigenomeDNA MethylationHistonesMitochondriaHistonesEpigenomeGene expressionMetabolismMitochondriaSignaling

Identifiers

PMID33271282
PMCPMC8166959
OpenAlexW3110525223

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.