Evidence map›Paper›PMID 16968212›Full record

ReviewAnnual review of pharmacology and toxicology2007

Diseases caused by defects in the visual cycle: retinoids as potential therapeutic agents.

Gabriel H Travis, Marcin Golczak, Alexander R Moise, Krzysztof Palczewski

Open access · greenAbstract readReview
In one paragraph

Review in Annual review of pharmacology and toxicology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 269 papers.

0numbers the graph read from it
0cells of the map it votes in
269citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

269 citing papers in PubMed, 415 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Illuminating retinoid flux in the neurosensory retina.The Journal of clinical investigation · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Therapeutic potential of allogeneic iPS cell-derived RPE transplantation forAmerican journal of ophthalmology case reports · 2025
    Article
  15. Article
  16. Light as a Mediator of Acute and Chronic Retina Degeneration.Advances in experimental medicine and biology · 2025
    Review
  17. Frontiers in ophthalmology · 2025
    Review
  18. In vivo photoreceptor base editing ameliorates rhodopsin-E150K autosomal-recessive retinitis pigmentosa in mice.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  19. Article
  20. Novel Therapeutic Effects ofPharmaceuticals (Basel, Switzerland) · 2024
    Article

209 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

4 authors at 2 institutions in 1 country.

Gabriel H TravisDepartment of Ophthalmology, UCLA School of Medicine, Los Angeles, CA 90095, USA. travis@jsei.ucla.edu
Marcin Golczak
Alexander R Moise
Krzysztof Palczewski
Case Western Reserve University · USUniversity of California, Los Angeles · US

Funding

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
The Role of Muller Cells in Visual Pigment RegenerationR01EY011713 · NEI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI TRAVIS, GABRIEL H · 1997 to 2017
$6.9M
Biochemical and Genetic Analysis of the Visual CycleR01EY015844 · NEI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TRAVIS, GABRIEL H · 2005 to 2009
$1.9M
NEI NIH HHS EY 015844NEI NIH HHS EY 09339NEI NIH HHS EY 11373NEI NIH HHS EY 11713NEI NIH HHS P30 EY011373NEI NIH HHS R01 EY009339NEI NIH HHS R01 EY011713NEI NIH HHS R01 EY015844
6 · The paper itself

Abstract

Absorption of a photon by an opsin pigment causes isomerization of the chromophore from 11-cis-retinaldehyde to all-trans-retinaldehyde. Regeneration of visual chromophore following light exposure is dependent on an enzyme pathway called the retinoid or visual cycle. Our understanding of this pathway has been greatly facilitated by the identification of disease-causing mutations in the genes coding for visual cycle enzymes. Defects in nearly every step of this pathway are responsible for human-inherited retinal dystrophies. These retinal dystrophies can be divided into two etiologic groups. One involves the impaired synthesis of visual chromophore. The second involves accumulation of cytotoxic products derived from all-trans-retinaldehyde. Gene therapy has been successfully used in animal models of these diseases to rescue the function of enzymes involved in chromophore regeneration, restoring vision. Dystrophies resulting from impaired chromophore synthesis can also be treated by supplementation with a chromophore analog. Dystrophies resulting from the accumulation of toxic pigments can be treated pharmacologically by inhibiting the visual cycle, or limiting the supply of vitamin A to the eyes. Recent progress in both areas provides hope that multiple inherited retinal diseases will soon be treated by pharmaceutical intervention.

Indexed as

AnimalsGenetic TherapyHumansModels, AnimalPhotoreceptor CellsRetinaRetinal DiseasesRetinoidsVision DisordersVitamin AVitaminsRetinoidsVitamin AVitamins

Identifiers

PMID16968212
PMCPMC2442882
OpenAlexW2171636319

What OpenQuestion holds

Textmetadata
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.