Retinoids and Retinal Diseases
Open accessAbstract
Recent progress in molecular understanding of the retinoid cycle in mammalian retina stems from painstaking biochemical reconstitution studies supported by natural or engineered animal models with known genetic lesions and studies of humans with specific genetic blinding diseases. Structural and membrane biology have been used to detect critical retinal enzymes and proteins and their substrates and ligands, placing them in a cellular context. These studies have been supplemented by analytical chemistry methods that have identified small molecules by their spectral characteristics, often in conjunction with the evaluation of models of animal retinal disease. It is from this background that rational therapeutic interventions to correct genetic defects or environmental insults are identified. Thus, most presently accepted modulators of the retinoid cycle already have demonstrated promising results in animal models of retinal degeneration. These encouraging signs indicate that some human blinding diseases can be alleviated by pharmacological interventions.
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Retinitis pigmentosa can be caused by dysfunctional LRAT, mutant RPE65, and P23H mutant opsin.
“Retinitis pigmentosa can be caused by dysfunctional LRAT, mutant RPE65, and P23H mutant opsin [52,58,59].”
From Vitamin A Transporters in Visual Function: A Mini Review on Membrane Receptors for Dietary Vitamin A Uptake, Storage, and Transport to the Eye (2021) · cites this paper as [52]
Section 5 states that loss-of-function LRAT mutations cause retinitis pigmentosa in humans, and Section 2 identifies P23H rhodopsin as a common cause of inherited autosomal dominant retinitis pigmentosa. Section 6 links RPE65 mutations to retinal degeneration and, in severe cases, Leber congenital amaurosis, but does not identify them as a cause of retinitis pigmentosa. Page numbers were not supplied in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe main visual chromophore responsible for vision that binds to opsin in photoreceptors is 11-cis retinal, a metabolite of vitamin A.
“The main visual chromophore responsible for the vision that binds to opsin in photoreceptors is 11-cis retinal, a metabolite of vitamin A, which was discovered to be important for vision in the late 1960s by George Wald, who also elucidated the visual or retinoid cycle involved with the metabolism of vitamin A in visual function [52].”
From Vitamin A Transporters in Visual Function: A Mini Review on Membrane Receptors for Dietary Vitamin A Uptake, Storage, and Transport to the Eye (2021) · cites this paper as [52]
11-cis retinal is transported from the RPE into the photoreceptors by interphotoreceptor RBP (IRBP) and binds to opsin in either the rods or cones.
“11-cis retinal is transported from the RPE into the photoreceptors by interphotoreceptor RBP (IRBP) and binds to opsin in either the rods or cones (forming rhodopsin or cone opsin, respectively) [52].”
From Vitamin A Transporters in Visual Function: A Mini Review on Membrane Receptors for Dietary Vitamin A Uptake, Storage, and Transport to the Eye (2021) · cites this paper as [52]
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- Authors
- Kiser, P. D., & Palczewski, K.
- Affiliations
- Louis Stokes Cleveland VA Medical Center (US)
- Case Western Reserve University (US)
- Venue
- Annual Review of Vision Science
- Publisher
- Annual Reviews
- Published
- 2016-10-14
- Volume
- 2
- Issue
- 1
- Pages
- 197-234
- ISSN
- 2374-4642 (ISSN-L)
- 2374-4650
- PMC
- PMC5132409
- OpenAlex
- W2214193457
- Semantic Scholar
- ad615b15ff3ffb755ccd22e081a92c5ab51af980
- Cited by
- 108
- References
- 175
- Citations by year
- 2026: 8 · 2025: 6 · 2024: 11 · 2023: 12 · 2022: 15 · 2021: 10 · 2020: 19 · 2019: 8 · 2018: 10 · 2017: 9
- FWCI
- 0.81
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Vision Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- U.S. Department of Veterans Affairs (IK2BX002683)
- Arnold and Mabel Beckman Foundation
- Foundation Fighting Blindness
- National Institutes of Health
- National Eye Institute (U01EY025451, R01EY009339)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Keywords
- retinoids, retinoid cycle, retinal degeneration, retinal disease, vitamin A metabolism, pharmacotherapy
- MeSH terms
- Animals, Disease Models, Animal, Humans, Retinal Diseases, Retinoids
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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