ArticleNature communications2018
Increased proteasomal activity supports photoreceptor survival in inherited retinal degeneration.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
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
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- The proteasome as a druggable target with multiple therapeutic potentialities: Cutting and non-cutting edges.Pharmacology & therapeutics · 2020Pooled it
- Stimulating proteasomal degradation in human proteinopathies.The FEBS journal · 2026Review
- Enhancing Experience-Dependent Plasticity Accelerates Vision Loss in a Murine Model of Retinitis Pigmentosa.Investigative ophthalmology & visual science · 2026Article
- Article
- Identification and validation of a novel ferroptosis-related gene signature associated with inherited retinal degeneration in Rd10 mice.Scientific reports · 2026Article
- Cryptochrome interaction networks across different tissues in Drosophila melanogaster.Biology direct · 2025Article
- Enhancing experience-dependent plasticity accelerates vision loss in a murine model of retinitis pigmentosa.bioRxiv : the preprint server for biology · 2025Article
- SON-dependent nuclear speckle rehabilitation alleviates proteinopathies.Nature communications · 2025Article
- Functional significance of commonly regulated genes in mechanically and chemically induced retinal ganglion cell death in rat eyes.Scientific reports · 2025Article
- Not Just PA28γ: What We Know About the Role of PA28αβ in Carcinogenesis.Biomolecules · 2025Review
- SON-dependent nuclear speckle rehabilitation alleviates proteinopathies.bioRxiv : the preprint server for biology · 2025Article
- Mechanisms of Rhodopsin-Related Inherited Retinal Degeneration and Pharmacological Treatment Strategies.Cells · 2025Review
- Promotion of endoplasmic reticulum retrotranslocation by overexpression of E3 ubiquitin-protein ligase synoviolin 1 reduces endoplasmic reticulum stress and preserves cone photoreceptors in cyclic nucleotide-gated channel deficiency.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Acyl-CoA synthetase 6 controls rod photoreceptor function and survival by shaping the phospholipid composition of retinal membranes.Communications biology · 2024Article
- Contribution of intraflagellar transport to compartmentalization and maintenance of the photoreceptor cell.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Aggregation of rhodopsin mutants in mouse models of autosomal dominant retinitis pigmentosa.Nature communications · 2024Article
- E3 ubiquitin ligase Herc3 deficiency leads to accumulation of subretinal microglia and retinal neurodegeneration.Scientific reports · 2024Article
- Therapeutic potential of archaeal unfoldase PANet and the gateless T20S proteasome in P23H rhodopsin retinitis pigmentosa mice.PloS one · 2024Article
- Article
- Losing, preserving, and restoring vision from neurodegeneration in the eye.Current biology : CB · 2023Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Inherited retinal degenerations, affecting more than 2 million people worldwide, are caused by mutations in over 200 genes. This suggests that the most efficient therapeutic strategies would be mutation independent, i.e., targeting common pathological conditions arising from many disease-causing mutations. Previous studies revealed that one such condition is an insufficiency of the ubiquitin-proteasome system to process misfolded or mistargeted proteins in affected photoreceptor cells. We now report that retinal degeneration in mice can be significantly delayed by increasing photoreceptor proteasomal activity. The largest effect is observed upon overexpression of the 11S proteasome cap subunit, PA28α, which enhanced ubiquitin-independent protein degradation in photoreceptors. Applying this strategy to mice bearing one copy of the P23H rhodopsin mutant, a mutation frequently encountered in human patients, quadruples the number of surviving photoreceptors in the inferior retina of 6-month-old mice. This striking therapeutic effect demonstrates that proteasomes are an attractive target for fighting inherited blindness.
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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.