ArticleBiomaterials2018
Genomic form of rhodopsin DNA nanoparticles rescued autosomal dominant Retinitis pigmentosa in the P23H knock-in mouse model.
Article in Biomaterials, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 29 citations in OpenAlex.
- Preclinical dose response study shows NR2E3 can attenuate retinal degeneration in the retinitis pigmentosa mouse model RhoGene therapy · 2024Article
- Gene augmentation for autosomal dominant retinitis pigmentosa using rhodopsin genomic loci nanoparticles in the P23HGene therapy · 2023Article
- Article
- Gene Therapy for Rhodopsin Mutations.Cold Spring Harbor perspectives in medicine · 2022Article
- A Modified Arrestin1 Increases Lactate Production in the Retina and Slows Retinal Degeneration.Human gene therapy · 2022Article
- Prospects of Non-Coding Elements in Genomic DNA Based Gene Therapy.Current gene therapy · 2022Review
- The Landscape of Non-Viral Gene Augmentation Strategies for Inherited Retinal Diseases.International journal of molecular sciences · 2021Review
- Neogenin neutralization prevents photoreceptor loss in inherited retinal degeneration.The Journal of clinical investigation · 2020Article
- Hepatocyte nuclear factor 4α negatively regulates connective tissue growth factor during liver regeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Rhodopsin Genomic Loci DNA Nanoparticles Improve Expression and Rescue of Retinal Degeneration in a Model for Retinitis Pigmentosa.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- A cerium oxide loaded glycol chitosan nano-system for the treatment of dry eye disease.Journal of controlled release : official journal of the Controlled Release Society · 2019Article
- Genome Editing as a Treatment for the Most Prevalent Causative Genes of Autosomal Dominant Retinitis Pigmentosa.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Retinitis pigmentosa (RP) is a group of inherited retinal degenerative conditions and a leading cause of irreversible blindness. 25%-30% of RP cases are caused by inherited autosomal dominant (ad) mutations in the rhodopsin (Rho) protein of the retina, which impose a barrier for developing therapeutic treatments for this genetically heterogeneous disorder, as simple gene replacement is not sufficient to overcome dominant disease alleles. Previously, we have explored using the genomic short-form of Rho (sgRho) for gene augmentation therapy of RP in a Rho knockout mouse model. We have shown improved gene expression and fewer epigenetic modifications compared with the use of a Rho cDNA expression construct. In the current study, we altered our strategy by delivering a codon-optimized genomic form of Rho (co-sgRho) (for gene replacement) in combination with an RNAi-based inactivation of endogenous Rho alleles (gene suppression of both mutant Rho alleles, but mismatched with the co-sgRho) into a homozygous Rho
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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.