Evidence map›Paper›PMID 25127496›Full record

ReviewEnvironmental health perspectives2014

Mitochondria, energetics, epigenetics, and cellular responses to stress.

Daniel T Shaughnessy, Kimberly McAllister, Leroy Worth, Astrid C Haugen, Joel N Meyer, Frederick E Domann, Bennett Van Houten, Raul Mostoslavsky, Scott J Bultman, Andrea A Baccarelli and 9 more

Open access · diamondAbstract readReview
In one paragraph

Review in Environmental health perspectives, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 5 pooled it
10.1field-weighted citation impact, top 1% 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

139 citing papers in PubMed, 5 syntheses or guidelines pooled it, 269 citations in OpenAlex.

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  16. Mitochondrial epigenetic mechanisms in cancer: an updated overview.Frontiers in cell and developmental biology · 2025
    Review
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79 more citing papers are in PubMed but not listed here.

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

19 authors at 12 institutions in 2 countries.

Daniel T ShaughnessyDivision of Extramural Research and Training, National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, North Carolina, USA.
Kimberly McAllister
Leroy Worth
Astrid C Haugen
Joel N Meyer
Frederick E Domann
Bennett Van Houten
Raul Mostoslavsky
Scott J Bultman
Andrea A Baccarelli
Thomas J Begley
Robert W Sobol
Matthew D Hirschey
Trey Ideker
Janine H Santos
William C Copeland
Raymond R Tice
David M Balshaw
Frederick L Tyson
National Institutes of Health · USTriangle · USDuke Medical Center · USDuke University · USHarvard University · USLaboratory of Molecular Genetics · PLPurchase College · USUniversity of California San Diego · USUniversity of Iowa · USUniversity of North Carolina at Chapel Hill · USUniversity of Pittsburgh · USUPMC Hillman Cancer Center · US

Funding

Zebrafish as a Detector of Organophosphate ExposureP42ES010356 · NIEHS · DUKE UNIVERSITY · PI AMY H HERRING · 2000 to 2026
$56.2M
Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Jong Sung Kim · 1990 to 2026
$40.5M
Molecular Characterization Of The Mitochondrial Dna PolymeraseZIAES065078 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI COPELAND, WILLIAM · 2009 to 2025
$25.4M
Studies on the Mechanisms by which SIRT5 Regulates Aging and DiseaseR01AG045351 · NIA · DUKE UNIVERSITY · PI HIRSCHEY, MATTHEW D · 2014 to 2023
$4.4M
Novel approaches to enhance tumor cell cytotoxicity of alkylating agentsR01CA148629 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SOBOL, ROBERT W · 2010 to 2021
$3.4M
The Role of Mitochondrial DNA Damage in NeurodegenerationR01ES017540 · NIEHS · DUKE UNIVERSITY · PI MEYER, JOEL NEWMAN · 2011 to 2015
$1.8M
Histone tails as an energy reservoir for mitochondrial functionR21ES025638 · NIEHS · MASSACHUSETTS GENERAL HOSPITAL · PI MOSTOSLAVSKY, RAUL · 2015 to 2017
$597k
Research and testing activities for the National Toxicology Program (NTP)ZIAES103227 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI TICE, RAYMOND · 2014 to 2014
$514k
NCI NIH HHS R01 CA148629NIA NIH HHS R01 AG045351NIEHS NIH HHS P30 ES005605NIEHS NIH HHS P42 ES010356NIEHS NIH HHS R01 ES017540NIEHS NIH HHS R21 ES025638
6 · The paper itself

Abstract

backgroundCells respond to environmental stressors through several key pathways, including response to reactive oxygen species (ROS), nutrient and ATP sensing, DNA damage response (DDR), and epigenetic alterations. Mitochondria play a central role in these pathways not only through energetics and ATP production but also through metabolites generated in the tricarboxylic acid cycle, as well as mitochondria-nuclear signaling related to mitochondria morphology, biogenesis, fission/fusion, mitophagy, apoptosis, and epigenetic regulation.

objectivesWe investigated the concept of bidirectional interactions between mitochondria and cellular pathways in response to environmental stress with a focus on epigenetic regulation, and we examined DNA repair and DDR pathways as examples of biological processes that respond to exogenous insults through changes in homeostasis and altered mitochondrial function.

methodsThe National Institute of Environmental Health Sciences sponsored the Workshop on Mitochondria, Energetics, Epigenetics, Environment, and DNA Damage Response on 25-26 March 2013. Here, we summarize key points and ideas emerging from this meeting. DISCUSSION: A more comprehensive understanding of signaling mechanisms (cross-talk) between the mitochondria and nucleus is central to elucidating the integration of mitochondrial functions with other cellular response pathways in modulating the effects of environmental agents. Recent studies have highlighted the importance of mitochondrial functions in epigenetic regulation and DDR with environmental stress. Development and application of novel technologies, enhanced experimental models, and a systems-type research approach will help to discern how environmentally induced mitochondrial dysfunction affects key mechanistic pathways.

conclusionsUnderstanding mitochondria-cell signaling will provide insight into individual responses to environmental hazards, improving prediction of hazard and susceptibility to environmental stressors.

Indexed as

Environmental ExposureDNA DamageDNA, MitochondrialEnvironmental PollutantsGenome, MitochondrialHumansMitochondriaDNA, MitochondrialEnvironmental Pollutants

Identifiers

PMID25127496
PMCPMC4256704
OpenAlexW2170201161

What OpenQuestion holds

Textmetadata
LicenceCC0
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.