Evidence map›Paper›PMID 34857922›Full record

ReviewNature reviews. Genetics2022

The potential of mitochondrial genome engineering.

Pedro Silva-Pinheiro, Michal Minczuk

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Genetics, 2022. 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
9.8field-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

85 citing papers in PubMed, 150 citations in OpenAlex.

  1. Review
  2. Article
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  6. Peptide-protein docking: from physics-based models to generative intelligence.Chemical communications (Cambridge, England) · 2026
    Review
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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

2 authors at 1 institution in 1 country.

Pedro Silva-PinheiroMRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-0872-5749
Michal MinczukMRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK. michal.minczuk@mrc-mbu.cam.ac.uk.ORCID http://orcid.org/0000-0001-8242-1420
University of Cambridge · GB

Funding

Medical Research Council MC_UU_00015/4Medical Research Council MC_UU_00015/7
6 · The paper itself

Abstract

Mitochondria are subject to unique genetic control by both nuclear DNA and their own genome, mitochondrial DNA (mtDNA), of which each mitochondrion contains multiple copies. In humans, mutations in mtDNA can lead to devastating, heritable, multi-system diseases that display different tissue-specific presentation at any stage of life. Despite rapid advances in nuclear genome engineering, for years, mammalian mtDNA has remained resistant to genetic manipulation, hampering our ability to understand the mechanisms that underpin mitochondrial disease. Recent developments in the genetic modification of mammalian mtDNA raise the possibility of using genome editing technologies, such as programmable nucleases and base editors, for the treatment of hereditary mitochondrial disease.

Indexed as

Genome, MitochondrialMitochondrial DiseasesAnimalsDNA, MitochondrialHumansMammalsMitochondriaMutationDNA, Mitochondrial

Identifiers

PMID34857922
OpenAlexW3216425243

What OpenQuestion holds

Textmetadata
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.