Evidence map›Paper›PMID 22198730›Full record

ArticleNature chemical biology2011

Primary amines protect against retinal degeneration in mouse models of retinopathies.

Akiko Maeda, Marcin Golczak, Yu Chen, Kiichiro Okano, Hideo Kohno, Satomi Shiose, Kaede Ishikawa, William Harte, Grazyna Palczewska, Tadao Maeda and 1 more

Abstract read
In one paragraph

Article in Nature chemical biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 2 pooled it
5.2field-weighted citation impact, top 4% 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

97 citing papers in PubMed, 2 syntheses or guidelines pooled it, 133 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Autosomal RecessiveInternational journal of molecular sciences · 2026
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  4. Review
  5. Advances and therapeutic opportunities in visual cycle modulation.Progress in retinal and eye research · 2025
    Review
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  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. 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
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Lipofuscin causes atypical necroptosis through lysosomal membrane permeabilization.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  19. Involvement of Oxidative and Endoplasmic Reticulum Stress inInternational journal of molecular sciences · 2021
    Article
  20. Review

37 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

11 authors at 2 institutions in 1 country.

Akiko MaedaDepartment of Ophthalmology and Visual Sciences, Case Western Reserve University, Cleveland, Ohio, USA.
Marcin Golczak
Yu Chen
Kiichiro Okano
Hideo Kohno
Satomi Shiose
Kaede Ishikawa
William Harte
Grazyna Palczewska
Tadao Maeda
Krzysztof Palczewski
Case Western Reserve University · USPolgenix (United States) · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024989 · NCRR · CASE WESTERN RESERVE UNIVERSITY · PI DAVIS, PAMELA B · 2007 to 2011
$53.7M
TISSUE CULTURE AND HYBRIDOMA MODULEP30EY011373 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI Irina A Pikuleva · 1997 to 2026
$17.7M
STRUCTURAL STUDIES OF ARRESTINSR01EY009339 · NEI · UNIVERSITY OF WASHINGTON · PI KISER, PHILIP DAVID, PALCZEWSKI, KRZYSZTOF · 1992 to 2025
$16.0M
Pharmacological Treatment of Retinal DiseasesR24EY021126 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI PALCZEWSKI, KRZYSZTOF · 2010 to 2014
$12.8M
Retinal degeneration diseases and the visual retinoid cycleK08EY019031 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI MAEDA, AKIKO · 2008 to 2012
$430k
Genetics and Therapy of Age-related Retinal Dysfunction in A/J MiceK08EY019880 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI MAEDA, TADAO · 2010 to 2013
$324k
NEI NIH HHS EY009339NEI NIH HHS EY019031NEI NIH HHS EY019880NEI NIH HHS EY021126NEI NIH HHS K08 EY019031NEI NIH HHS K08 EY019880NEI NIH HHS P30 EY011373NEI NIH HHS P30 EY11373NEI NIH HHS R01 EY009339NEI NIH HHS R24 EY021126
6 · The paper itself

Abstract

Vertebrate vision is initiated by photoisomerization of the visual pigment chromophore 11-cis-retinal and is maintained by continuous regeneration of this retinoid through a series of reactions termed the retinoid cycle. However, toxic side reaction products, especially those involving reactive aldehyde groups of the photoisomerized product, all-trans-retinal, can cause severe retinal pathology. Here we lowered peak concentrations of free all-trans-retinal with primary amine-containing Food and Drug Administration (FDA)-approved drugs that did not inhibit chromophore regeneration in mouse models of retinal degeneration. Schiff base adducts between all-trans-retinal and these amines were identified by MS. Adducts were observed in mouse eyes only when an experimental drug protected the retina from degeneration in both short-term and long-term treatment experiments. This study demonstrates a molecular basis of all-trans-retinal-induced retinal pathology and identifies an assemblage of FDA-approved compounds with protective effects against this pathology in a mouse model that shows features of Stargardt's disease and age-related retinal degeneration.

Indexed as

AminesAnimalsDisease Models, AnimalDose-Response Relationship, DrugMacular DegenerationMiceRetinal DegenerationRetinaldehydeSchiff BasesUnited StatesUnited States Food and Drug AdministrationAminesRetinaldehydeSchiff Bases

Identifiers

PMID22198730
PMCPMC3518042
OpenAlexW2004577874

What OpenQuestion holds

Textmetadata
LicenceTDM
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.