Evidence map›Paper›PMID 35315776›Full record

ArticleeLife2022

Retinoic acid signaling mediates peripheral cone photoreceptor survival in a mouse model of retina degeneration.

Ryoji Amamoto, Grace K Wallick, Constance L Cepko

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
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  4. RPE-specific MCT2 expression promotes cone survival in models of retinitis pigmentosa.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  9. Ablation of Fatty Acid Transport Protein-4 Enhances Cone Survival, M-cone Vision, and Synthesis of Cone-Tropic 9-The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  10. Article
  11. Article
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  13. Chromophore supply modulates cone function and survival in retinitis pigmentosa mouse models.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. 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

3 authors at 1 institution in 1 country.

Ryoji AmamotoDepartment of Genetics and Ophthalmology, Howard Hughes Medical Institute, Blavatnik Institute, Harvard Medical School, Boston, United States.ORCID 0000-0002-9335-112X
Grace K WallickDepartment of Genetics and Ophthalmology, Howard Hughes Medical Institute, Blavatnik Institute, Harvard Medical School, Boston, United States.
Constance L CepkoDepartment of Genetics and Ophthalmology, Howard Hughes Medical Institute, Blavatnik Institute, Harvard Medical School, Boston, United States.ORCID 0000-0002-9945-6387
Howard Hughes Medical Institute · US

Funding

Elucidating the molecular and cellular mechanisms underlying cone survival in the peripheral retina in mouse models of Retinitis PigmentosaK99EY032110 · NEI · HARVARD MEDICAL SCHOOL · PI AMAMOTO, RYOJI · 2021 to 2022
$178k
Howard Hughes Medical InstituteNEI NIH HHS K99 EY032110
6 · The paper itself

Abstract

Retinitis Pigmentosa (RP) is a progressive, debilitating visual disorder caused by mutations in a diverse set of genes. In both humans with RP and mouse models of RP, rod photoreceptor dysfunction leads to loss of night vision, and is followed by secondary cone photoreceptor dysfunction and degeneration, leading to loss of daylight color vision. A strategy to prevent secondary cone death could provide a general RP therapy to preserve daylight color vision regardless of the underlying mutation. In mouse models of RP, cones in the peripheral retina survive long-term, despite complete rod loss. The mechanism for such peripheral cone survival had not been explored. Here, we found that active retinoic acid (RA) signaling in peripheral Muller glia is necessary for the abnormally long survival of these peripheral cones. RA depletion by conditional knockout of RA synthesis enzymes, or overexpression of an RA degradation enzyme, abrogated the extended survival of peripheral cones. Conversely, constitutive activation of RA signaling in the central retina promoted long-term cone survival. These results indicate that RA signaling mediates the prolonged peripheral cone survival in the rd1 mouse model of retinal degeneration, and provide a basis for a generic strategy for cone survival in the many diseases that lead to loss of cone-mediated vision.

Indexed as

Color VisionRetinal DegenerationRetinitis PigmentosaAnimalsDisease Models, AnimalMiceRetinaRetinal Cone Photoreceptor CellsTretinoinTretinoinconesdegenerationdevelopmental biologymouseneurosciencephotoreceptorretinaretinitis pigmentosa

Identifiers

PMID35315776
PMCPMC8940176
OpenAlexW4221007578

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.