ArticleInvestigative ophthalmology & visual science2025
Dynamic Inner Blood Retina Barrier Disruption in Retinitis Pigmentosa.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Retinitis pigmentosa (RP) is the most common and genetically heterogenous inherited retinal degeneration described. Although vascular attenuation is a notable phenotype in later stages of the disease, the temporal nature of this attenuation and its contribution to disease are not well understood. Despite a growing body of research suggesting that blood-brain barrier (BBB) disruption can drive neurological deficits across a wide range of conditions, there is a paucity of data related to the contribution of inner blood-retina barrier (iBRB) disruption in RP. Methods: Here, we sought to examine retinal vascular changes in three established mouse models of RP, Rho-/-, Rd10, and Rpe65D477G. Each model was also established on a claudin-5 heterozygous (Cldn5+/-) background to examine retinal pathology in the context of a "leaky" iBRB. Additionally, we quantitatively examined iBRB integrity in patients with RP (n = 14) harboring autosomal dominant variants in either the RHO or RPE65 genes. Results: Our results show decreased perfusion capacity and disruptions to retinal vascular plexuses within these models, highlighting a perturbed vascular state across Rho-/-, Rd10, and Rpe65D477G models. We highlight a specific loss of the deeper vascular plexus in more rapidly degenerating Rho-/- and Rd10 models, while still observing a global loss of CLDN5 vascular coverage in Rpe65D477G models despite lack of deep plexus degeneration. Moreover, our novel retinal degenerative models on a background of Cldn5 heterozygosity allow us to investigate retinal pathology of these models in the context of a "leaky" iBRB and highlight a specific sensitivity of the larger retinal macrovessels in these models. Furthermore, we find similar phenotypic patterns in a cohort of patients with RP with temporal iBRB changes that phenocopy these preclinical models. Conclusions: Cumulatively, these findings represent the first quantitative profiling of iBRB disruption in RP and suggest that retinal vascular stabilization may represent a gene agnostic approach to treating this devastating form of blindness.
Indexed as
Identifiers
What OpenQuestion holds
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.