ArticleJournal of ophthalmology2011
Regulation of posttranscriptional modification as a possible therapeutic approach for retinal neuroprotection.
Article in Journal of ophthalmology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed, 25 citations in OpenAlex.
- Diabetic retinopathy: shaped by the "hidden hand" of post-translational modifications.Molecular neurodegeneration · 2026Review
- Causal relevance of the JAK/STAT pathway for cardioprotection via cold acclimation.Scientific reports · 2026Article
- The CD39-CD73-adenosine axis: a pivotal regulator of retinal homeostasis and diseases.Frontiers in cell and developmental biology · 2026Review
- Ocular Vascular Diseases: From Retinal Immune Privilege to Inflammation.International journal of molecular sciences · 2023Review
- Telomere Lengths and Serum Proteasome Concentrations in Patients with Type 1 Diabetes and Different Severities of Diabetic Retinopathy in Latvia and Lithuania.Journal of clinical medicine · 2022Article
- Review
- Immunosubunit β5i Knockout Suppresses Neovascularization and Restores Autophagy in Retinal Neovascularization by Targeting ATG5 for Degradation.Investigative ophthalmology & visual science · 2020Article
- Neuroprotective Peptides in Retinal Disease.Journal of clinical medicine · 2019Review
- Relationships Between Neurodegeneration and Vascular Damage in Diabetic Retinopathy.Frontiers in neuroscience · 2019Review
- Neuroprotective effect of activated 5'-adenosine monophosphate-activated protein kinase on cone system function during retinal inflammation.BMC neuroscience · 2016Article
- The Neuroprotective Effect of Rapamycin as a Modulator of the mTOR-NF-κB Axis during Retinal Inflammation.PloS one · 2016Article
- E3 ubiquitin ligase Siah-1 downregulates synaptophysin expression under high glucose and hypoxia.American journal of translational research · 2015Article
- Article
- The ubiquitin-proteasome system in retinal health and disease.Molecular neurobiology · 2013Review
- Neuroprotective effects of lutein in the retina.Current pharmaceutical design · 2012Review
- Renin-Angiotensin system hyperactivation can induce inflammation and retinal neural dysfunction.International journal of inflammation · 2012Article
- Neural degeneration in the retina of the streptozotocin-induced type 1 diabetes model.Experimental diabetes research · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding pathogenesis at the molecular level is the first step toward developing new therapeutic approaches. Here, we review the molecular mechanisms of visual dysfunction in two common diseases, innate chorioretinal inflammation and diabetic retinopathy, and the role of the ubiquitin-proteasome system (UPS) in both processes. In innate chorioretinal inflammation, interleukin-6 family ligands induce STAT3 activation in photoreceptors, which causes UPS-mediated excessive degradation of the visual substance, rhodopsin. In diabetic retinopathy, angiotensin II type 1 receptor (AT1R) signaling activates ERK in the inner layers of the retina, causing UPS-mediated excessive degradation of the synaptic vesicle protein, synaptophysin. This latter effect may decrease synaptic activity, in turn adversely affecting neuronal survival. Both mechanisms involve increased UPS activity and the subsequent excessive degradation of a protein required for visual function. Finally, we review the therapeutic potential of regulating the UPS to protect tissue function, citing examples from clinical applications in other medical fields.
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.