ArticleHuman gene therapy2022
A Modified Arrestin1 Increases Lactate Production in the Retina and Slows Retinal Degeneration.
Article in Human gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 12 citations in OpenAlex.
- Quercetin improves retinal glycolysis to slow myopia progression through orchestrating the AKT/FOXO/HK2 axis.Redox biology · 2026Article
- Metabolomic signatures suggest altered bile acid and energy metabolism in CRB1- retinopathies.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Enhancing Experience-Dependent Plasticity Accelerates Vision Loss in a Murine Model of Retinitis Pigmentosa.Investigative ophthalmology & visual science · 2026Article
- Arrestins as Possible Drug Targets.Biomolecules & therapeutics · 2025Review
- Pten Loss Triggers Progressive Photoreceptor Degeneration in an mTORC1-Independent Manner.Investigative ophthalmology & visual science · 2025Article
- GPCR-dependent and -independent arrestin signaling.Trends in pharmacological sciences · 2024Review
- Arrestins: A Small Family of Multi-Functional Proteins.International journal of molecular sciences · 2024Review
- Unlocking the role of lactate: metabolic pathways, signaling, and gene regulation in postmitotic retinal cells.Frontiers in ophthalmology · 2023Review
- Gene Therapy for Rhodopsin Mutations.Cold Spring Harbor perspectives in medicine · 2022Article
- Beyond Genetics: The Role of Metabolism in Photoreceptor Survival, Development and Repair.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Glucose metabolism in the retina is carefully orchestrated, with glucose being delivered to photoreceptors from the choroidal circulation through the retinal pigmented epithelium (RPE). In photoreceptors, glucose is processed principally by aerobic glycolysis, from which the lactate byproduct is provided to the RPE and Müller glia for their energetic needs. In this study, we utilize a modified arrestin1 protein to enhance the glycolytic output of lactate from rod photoreceptors through disinhibition of enolase1 activity with the goal being to use this increased lactate production as a gene-agnostic approach to slowing retinal degeneration. Mouse arrestin1 with E362G/D363G amino acid substitutions (referred to as "ArrGG") was packaged into AAV and tested for safety and for efficacy in increasing retinal lactate production. Overexpression of ArrGG in C57BL/6J mice did not result in any detectable changes in either electroretinogram (ERG) function or photoreceptor survival as measured by outer nuclear layer (ONL) thickness. However, mouse retinas expressing ArrGG showed a ∼25% increase in the rate of lactate secretion. Therefore, AAV-ArrGG was delivered intravitreally to heterozygous P23H rhodopsin knockin mice (
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Registered trials
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.