Evidence map›Paper›PMID 27814659›Full record

ReviewFrontiers in bioscience (Landmark edition)2017

Current strategies towards therapeutic manipulation of mtDNA heteroplasmy.

Claudia V Pereira, Carlos T Moraes

Open access · greenAbstract readReview
In one paragraph

Review in Frontiers in bioscience (Landmark edition), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Current advances in gene therapy of mitochondrial diseases.Journal of translational medicine · 2022
    Review
  9. Review
  10. Review
  11. Article
  12. Cellular mechanisms of mtDNA heteroplasmy dynamics.Critical reviews in biochemistry and molecular biology · 2021
    Review
  13. Article
  14. Manipulating and elucidating mitochondrial gene expression with engineered proteins.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Review
  15. Human mitochondrial nucleases.The FEBS journal · 2017
    Review
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 at 1 institution in 1 country.

Claudia V PereiraDepartment of Neurology, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Carlos T MoraesDepartment of Neurology, University of Miami Miller School of Medicine, Miami, FL 33136, USA, cmoraes@med.miami.edu.
University of Miami · US

Funding

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 R01 EY010804NIA NIH HHS R01 AG036871NIEHS NIH HHS R33 ES025673NINDS NIH HHS R01 NS079965
6 · The paper itself

Abstract

Mitochondrial disease is a multifactorial disorder involving both nuclear and mitochondrial genomes. Over the past 20 years, great progress was achieved in the field of gene editing which raised the possibility of partial or complete elimination of mutant mtDNA that causes disease phenotypes. Each cell contains thousands of copies of mtDNA which can be either wild-type (WT) or mutant, a condition called heteroplasmy. As there are multiple copies of mtDNA inside a cell, the percentage of mutant mtDNA can vary and a directional shift in the heteroplasmy ratio towards an increase of WT mtDNA copies would have therapeutic value. Gene editing tools have been adapted to translocate to mitochondria and were able to change heteroplasmy in a predictable manner. These include mitochondrial targeted restriction endonucleases, Zinc-finger nucleases, and TAL-effector nucleases. These procedures could also be adapted to reduce the levels of mutant mtDNA in embryos, offering an option to the controversial mitochondrial replacement techniques during

Indexed as

MutationAnimalsDNA, MitochondrialDNA Restriction EnzymesEnergy MetabolismFemaleGene EditingGerm-Line MutationHumansMaleMaternal InheritanceMitochondriaMitochondrial DiseasesMitosisModels, GeneticTranscription Activator-Like Effector NucleasesDNA, MitochondrialDNA Restriction EnzymesTranscription Activator-Like Effector Nucleases

Identifiers

PMID27814659
PMCPMC6986768
OpenAlexW2547539639

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.