Evidence map›Paper›PMID 29281123›Full record

ReviewFEBS letters2018

Mitochondrial DNA damage and reactive oxygen species in neurodegenerative disease.

Nadee Nissanka, Carlos T Moraes

Abstract readReview
In one paragraph

Review in FEBS letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 253 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
253citing papers in PubMed, 1 pooled it
–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

253 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
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  12. Article
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  14. Article
  15. CypD Dependent mPTP Opening Is Crucial for Oxidized Mitochondrial DNA Release in Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  16. Review
  17. Review
  18. Ultrasonic exposure enhances the body's antioxidant capacity.Journal of clinical biochemistry and nutrition · 2026
    Article
  19. Article
  20. Review

193 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

2 authors.

Nadee NissankaNeuroscience Graduate Program, University of Miami Miller School of Medicine, FL, USA.
Carlos T MoraesNeuroscience Graduate Program, University of Miami Miller School of Medicine, FL, USA.

Funding

Shared Equipment ModuleP30EY014801 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Victor L Perez · 2004 to 2026
$12.2M
SETTING THE STAGE FOR REPLACEMENT OF MITOCHONDRIAL GENESR01EY010804 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 1995 to 2025
$9.4M
Cellular and Molecular Consequences of Respiratory Chain Defects in NeuronsR01NS079965 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 2012 to 2023
$3.9M
Mitochondrial Dysfunction in Neurodegeneration and Compensatory ApproachesR01AG036871 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 2010 to 2020
$3.3M
Imaging mitochondrial signaling in B-cells ectopically implanted in the eyeR33ES025673 · NIEHS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI CAICEDO, ALEJANDRO, MORAES, CARLOS TORRES · 2018 to 2019
$761k
NEI NIH HHS P30 EY014801NEI NIH HHS R01 EY010804NIA NIH HHS R01 AG036871NIEHS NIH HHS R33 ES025673NINDS NIH HHS R01 NS079965
6 · The paper itself

Abstract

Mitochondria are essential organelles within the cell where most ATP is produced through oxidative phosphorylation (OXPHOS). A subset of the genes needed for this process are encoded by the mitochondrial DNA (mtDNA). One consequence of OXPHOS is the production of mitochondrial reactive oxygen species (ROS), whose role in mediating cellular damage, particularly in damaging mtDNA during ageing, has been controversial. There are subsets of neurons that appear to be more sensitive to ROS-induced damage, and mitochondrial dysfunction has been associated with several neurodegenerative disorders. In this review, we will discuss the current knowledge in the field of mtDNA and neurodegeneration, the debate about ROS as a pathological or beneficial contributor to neuronal function, bona fide mtDNA diseases, and insights from mouse models of mtDNA defects affecting the central nervous system.

Indexed as

DNA DamageAnimalsDNA, MitochondrialHumansNeurodegenerative DiseasesOxidative PhosphorylationReactive Oxygen SpeciesDNA, MitochondrialReactive Oxygen Speciesmitochondrial DNAneurodegenerationreactive oxygen species

Identifiers

PMID29281123
PMCPMC6942696

What OpenQuestion holds

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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.