Evidence map›Paper›PMID 39177028›Full record

ArticleeLife2024

Yohei Nitta, Jiro Osaka, Ryuto Maki, Satoko Hakeda-Suzuki, Emiko Suzuki, Satoshi Ueki, Takashi Suzuki, Atsushi Sugie

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2024. 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. Novel in vivo models of autosomal optic atrophy reveal conserved pathological changes in neuronal mitochondrial structure and function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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

8 authors.

Yohei Nitta *Brain Research Institute, Niigata University, Niigata, Japan.ORCID https://orcid.org/0000-0002-0712-428X
Jiro Osaka *Brain Research Institute, Niigata University, Niigata, Japan.ORCID https://orcid.org/0009-0008-8015-1955
Ryuto MakiSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.
Satoko Hakeda-SuzukiSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.
Emiko SuzukiDepartment of Biological Sciences, Graduate School of Science, Tokyo Metropolitan University, Hachioji, Japan.ORCID https://orcid.org/0000-0002-4005-0542
Satoshi UekiDivision of Ophthalmology and Visual Science, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan.
Takashi SuzukiSchool of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.ORCID https://orcid.org/0000-0001-9093-2562
Atsushi SugieBrain Research Institute, Niigata University, Niigata, Japan.ORCID https://orcid.org/0000-0002-2090-8839

Funding

GSK Japan Research Grant 2022 AS2021A000166849Japan Agency for Medical Research and Development JP22ek019484sJapan Agency for Medical Research and Development JP24ek0109760s4001Japan Society for the Promotion of Science 16H06457Japan Society for the Promotion of Science 17H04983Japan Society for the Promotion of Science 18J00367Japan Society for the Promotion of Science 18K14835Japan Society for the Promotion of Science 19K22592Japan Society for the Promotion of Science 21H02483Japan Society for the Promotion of Science 21H02837Japan Society for the Promotion of Science 21H05682Japan Society for the Promotion of Science 21K06184Japan Society for the Promotion of Science 21K15619Japan Society for the Promotion of Science 24K02349Japan Society for the Promotion of Science 24K22104Takeda Science Foundation Bioscience Research GrantTakeda Science Foundation Life Science Research GrantTakeda Science Foundation Visionary Research Grant
6 · The paper itself

Abstract

Autosomal dominant optic atrophy (DOA) is a progressive form of blindness caused by degeneration of retinal ganglion cells and their axons, mainly caused by mutations in the OPA1 mitochondrial dynamin

Indexed as

Disease Models, AnimalDrosophila ProteinsGTP PhosphohydrolasesOptic Atrophy, Autosomal DominantAnimalsDrosophilaDrosophila melanogasterHumansMembrane ProteinsMutationDrosophila ProteinsGTP PhosphohydrolasesMembrane ProteinsOPA1 protein, DrosophilaOPA1 protein, humanaxonal degenerationD. melanogasterdominant optic atrophyDrosophilamedicineOPA1

Identifiers

PMID39177028
PMCPMC11343565

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.