Evidence map›Paper›PMID 39406814›Full record

ArticleScientific reports2024

Hypoxia-mediated rescue of retinal ganglion cells deficient in mitochondrial complex I is independent of the hypoxia-inducible factor pathway.

Alexander M Warwick, Howard M Bomze, Luyu Wang, Ying Hao, Sandra S Stinnett, Sidney M Gospe

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 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. Mitochondrial complex I deficiency-associated diseases and models.Cellular and molecular life sciences : CMLS · 2026
    Review
  2. 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

6 authors.

Alexander M WarwickDepartment of Ophthalmology, Duke University School of Medicine, Durham, NC, 27710, USA.
Howard M BomzeDepartment of Ophthalmology, Duke University School of Medicine, Durham, NC, 27710, USA.
Luyu WangDepartment of Ophthalmology, Duke University School of Medicine, Durham, NC, 27710, USA.
Ying HaoDepartment of Ophthalmology, Duke University School of Medicine, Durham, NC, 27710, USA.
Sandra S StinnettDepartment of Ophthalmology, Duke University School of Medicine, Durham, NC, 27710, USA.
Sidney M GospeDepartment of Ophthalmology, Duke University School of Medicine, Durham, NC, 27710, USA. smg4@duke.edu.

Funding

VISION RESEARCHP30EY005722 · NEI · DUKE UNIVERSITY · PI MALEK, GOLDIS · 1985 to 2025
$17.7M
In Vivo Modeling of Mitochondrial Complex I Deficiency in Retinal Ganglion CellsK08EY028610 · NEI · DUKE UNIVERSITY · PI GOSPE, SIDNEY M · 2018 to 2022
$856k
NEI NIH HHS EY005722NEI NIH HHS EY028610NEI NIH HHS K08 EY028610NEI NIH HHS P30 EY005722School of Medicine, Duke University Strong Start Award
6 · The paper itself

Abstract

Continuous exposure to environmental hypoxia (11% O

Indexed as

Basic Helix-Loop-Helix ProteinsElectron Transport Complex IHypoxia-Inducible Factor 1, alpha SubunitRetinal Ganglion CellsAnimalsDisease Models, AnimalEndothelial PAS Domain-Containing Protein 1HypoxiaMiceMice, KnockoutMitochondriaMitochondrial DiseasesSignal TransductionVon Hippel-Lindau Tumor Suppressor ProteinBasic Helix-Loop-Helix ProteinsElectron Transport Complex IEndothelial PAS Domain-Containing Protein 1Hif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitNdufs4 protein, mouseVHL protein, mouseVon Hippel-Lindau Tumor Suppressor ProteinComplex IHypoxiaHypoxia-inducible factorLeber hereditary optic neuropathyMitochondriaRetinal ganglion cell

Identifiers

PMID39406814
PMCPMC11480089

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.