Evidence map›Paper›PMID 18941295›Full record

ReviewProceedings of the Japan Academy. Series B, Physical and biological sciences2008

Reverse genetic studies of mitochondrial DNA-based diseases using a mouse model.

Kazuto Nakada, Akitsugu Sato, Jun-Ichi Hayashi

Abstract readReview
In one paragraph

Review in Proceedings of the Japan Academy. Series B, Physical and biological sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. Article
  2. Physiology and pathophysiology of mitochondrial DNA.Advances in experimental medicine and biology · 2012
    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

3 authors.

Kazuto NakadaGraduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Japan.
Akitsugu Sato
Jun-Ichi Hayashi

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the situation that it would not be able to produce model animals for mitochondrial diseases caused by mitochondrial DNA (mtDNA) with pathogenic mutations, we succeeded in generating mice with pathogenic deletion mutant mtDNA (DeltamtDNA), named "mito-mice", by direct introduction of mitochondria with DeltamtDNA into mouse zygotes. In the mito-mice, accumulation of DeltamtDNA induced mitochondrial respiration defects in various tissues, resulting in mitochondrial disease phenotypes, such as low body weight, lactic acidosis, ischemia, myopathy, heart block, deafness, male infertility, and renal failure. Thus, mito-mice are the first model animal for mtDNA-based diseases, and the mice could be valuable for understanding precise pathogeneses and testing therapies of mitochondrial diseases. In the present review, we summarized reverse genetic studies using the mito-mice.(Communicated by Takao SEKIYA, M.J.A.).

Indexed as

Disease Models, AnimalAnimalsDNA, MitochondrialMiceMitochondrial DiseasesMutationDNA, Mitochondrial

Identifiers

PMID18941295
PMCPMC2858368

What OpenQuestion holds

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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.