Evidence map›Paper›PMID 31335990›Full record

ReviewEnvironmental and molecular mutagenesis2019

Mitochondrial DNA: Epigenetics and environment.

Nidhi Sharma, Monica S Pasala, Aishwarya Prakash

Open access · greenAbstract readReview
In one paragraph

Review in Environmental and molecular mutagenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

85 citing papers in PubMed, 160 citations in OpenAlex.

  1. Article
  2. Review
  3. Mitochondria-targeted delivery strategies for age-related diseases.International journal of pharmaceutics: X · 2026
    Review
  4. Review
  5. Review
  6. Article
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  20. Review

25 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

3 authors at 2 institutions in 1 country.

Nidhi SharmaDepartment of Biochemistry and Molecular Biology, Mitchell Cancer Institute, The University of South Alabama, Mobile, Alabama.
Monica S PasalaDepartment of Biochemistry and Molecular Biology, Mitchell Cancer Institute, The University of South Alabama, Mobile, Alabama.
Aishwarya PrakashDepartment of Biochemistry and Molecular Biology, Mitchell Cancer Institute, The University of South Alabama, Mobile, Alabama.
USA Mitchell Cancer Institute · USUniversity of South Alabama · US

Funding

Repair of Environmentally Induced Mitochondrial DNA DamageR01ES030084 · NIEHS · UNIVERSITY OF SOUTH ALABAMA · PI PRAKASH, AISHWARYA · 2019 to 2023
$2.3M
Repair of Environmentally and Endogenously Induced Mitochondrial-DNA DamageR00ES024417 · NIEHS · UNIVERSITY OF SOUTH ALABAMA · PI PRAKASH, AISHWARYA · 2016 to 2018
$747k
NIEHS NIH HHS 1R01ES030084-01NIEHS NIH HHS 5R00ES024417-04NIEHS NIH HHS R00 ES024417NIEHS NIH HHS R01 ES030084
6 · The paper itself

Abstract

Maintenance of the mitochondrial genome is essential for proper cellular function. For this purpose, mitochondrial DNA (mtDNA) needs to be faithfully replicated, transcribed, translated, and repaired in the face of constant onslaught from endogenous and environmental agents. Although only 13 polypeptides are encoded within mtDNA, the mitochondrial proteome comprises over 1500 proteins that are encoded by nuclear genes and translocated to the mitochondria for the purpose of maintaining mitochondrial function. Regulation of mtDNA and mitochondrial proteins by epigenetic changes and post-translational modifications facilitate crosstalk between the nucleus and the mitochondria and ultimately lead to the maintenance of cellular health and homeostasis. DNA methyl transferases have been identified in the mitochondria implicating that methylation occurs within this organelle; however, the extent to which mtDNA is methylated has been debated for many years. Mechanisms of demethylation within this organelle have also been postulated, but the exact mechanisms and their outcomes is still an active area of research. Mitochondrial dysfunction in the form of altered gene expression and ATP production, resulting from epigenetic changes, can lead to various conditions including aging-related neurodegenerative disorders, altered metabolism, changes in circadian rhythm, and cancer. Here, we provide an overview of the epigenetic regulation of mtDNA via methylation, long and short noncoding RNAs, and post-translational modifications of nucleoid proteins (as mitochondria lack histones). We also highlight the influence of xenobiotics such as airborne environmental pollutants, contamination from heavy metals, and therapeutic drugs on mtDNA methylation. Environ. Mol. Mutagen., 60:668-682, 2019. © 2019 Wiley Periodicals, Inc.

Indexed as

DNA MethylationDNA, MitochondrialDNA ReplicationEpigenesis, GeneticGenome, MitochondrialHumansMitochondriaProtein Processing, Post-TranslationalRNA, UntranslatedDNA, MitochondrialRNA, Untranslatedmitochondrial epigeneticsmitochondrial post-translational modificationsmtDNA methylationnoncoding RNAsxenobiotics

Identifiers

PMID31335990
PMCPMC6941438
OpenAlexW2962964440

What Socratic 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 Socratic graph.