Evidence map›Paper›PMID 36001180›Full record

ReviewAnnals of biomedical engineering2024

Modulating Mitochondrial DNA Heteroplasmy with Mitochondrially Targeted Endonucleases.

Nikita Mikhailov, Riikka H Hämäläinen

Open access · hybridAbstract readReview
In one paragraph

Review in Annals of biomedical engineering, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
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  3. Review
  4. Article
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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

2 authors at 1 institution in 1 country.

Nikita MikhailovA.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211, Kuopio, Finland.
Riikka H HämäläinenA.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211, Kuopio, Finland. riikka.martikainen@uef.fi.ORCID http://orcid.org/0000-0002-5102-0672
University of Eastern Finland · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria, mainly known as energy factories of eukaryotic cells, also exert several additional signaling and metabolic functions and are today recognized as major cellular biosynthetic and signaling hubs. Mitochondria possess their own genome (mitochondrial DNA-mtDNA), that encodes proteins essential for oxidative phosphorylation, and mutations in it are an important contributor to human disease. The mtDNA mutations often exist in heteroplasmic conditions, with both healthy and mutant versions of the mtDNA residing in patients' cells and the level of mutant mtDNA may vary between different tissues and organs and affect the clinical outcome of the disease. Thus, shifting the ratio between healthy and mutant mtDNA in patients' cells provides an intriguing therapeutic option for mtDNA diseases. In this review we describe current strategies for modulating mitochondrial heteroplasmy levels with engineered endonucleases including mitochondrially targeted TALENs and Zinc finger nucleases (ZFNs) and discuss their therapeutic potential. These gene therapy tools could in the future provide therapeutic help both for patients with mitochondrial disease as well as in preventing the transfer of pathogenic mtDNA mutations from a mother to her offspring.

Indexed as

DNA, MitochondrialAnimalsEndonucleasesGenetic TherapyHeteroplasmyHumansMitochondriaMitochondrial DiseasesMutationTranscription Activator-Like Effector NucleasesZinc Finger NucleasesDNA, MitochondrialEndonucleasesTranscription Activator-Like Effector NucleasesZinc Finger NucleasesGene therapyGenetic engineeringmitoTALENOxidative phosphorylationRestriction endonucleaseZinc finger nuclease

Identifiers

PMID36001180
PMCPMC11329604
OpenAlexW4292953605

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.