ReviewAdvances in experimental medicine and biology2025
Ocular Tissue-Specific Amino Acid Metabolism in Gyrate Atrophy.
Review in Advances in experimental medicine and biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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.
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Who cites it
1 citing paper in PubMed.
- Early proteomic and metabolic signatures of liver and eye in OAT-deficient mice.Experimental eye research · 2026Article
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Authors and funding
3 authors.
Funding
Abstract
Deficiency of the mitochondrial enzyme ornithine aminotransferase (OAT) causes gyrate atrophy of the choroid and retina (GACR), a rare autosomal inherited disorder characterized by a substantial elevation in plasma ornithine and progressive chorioretinal degeneration. While OAT is expressed in many tissues, the deficiency mainly affects the retinal pigment epithelium (RPE)/choroid and retina, progressing from the periphery to the macula. RPE has been identified as the initial site of damage in GACR. Amino acid metabolism is crucial for the RPE function and its support for retinal metabolism. In GACR, in addition to ornithine, the metabolism of multiple amino acids is disrupted. This review explores the tissue-specific differences in amino acid metabolism between macular and peripheral ocular regions that may contribute to the pathophysiology of the disease.
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Registered trials
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