ArticleCell death & disease2019
Delineating the role of eIF2α in retinal degeneration.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 8 citations in OpenAlex.
- Unravelling genotype-phenotype correlations in Stargardt disease using patient-derived retinal organoids.Cell death & disease · 2025Article
- The endoplasmic reticulum: Homeostasis and crosstalk in retinal health and disease.Progress in retinal and eye research · 2024Review
- Retinal injury mouse model and pathophysiological assessment of the effect of arsenical vesicants.Experimental eye research · 2023Article
- GADD34 Ablation Exacerbates Retinal Degeneration in P23H RHO Mice.International journal of molecular sciences · 2022Article
- Targeting the integrated stress response in ophthalmology.Current eye research · 2021Review
- Endoplasmic reticulum stress: New insights into the pathogenesis and treatment of retinal degenerative diseases.Progress in retinal and eye research · 2020Review
- Inhibition of eIF2BioMed research international · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Activation of the unfolded protein response has been detected in various animal models of retinal degeneration. The PERK branch converges on eIF2α to regulate protein synthesis. We previously reported that diseased retinas produce less protein as they degenerate. We also proposed that the majority of this reduction in protein synthesis may not be due to control of eIF2α. Nevertheless, multiple research groups have reported that modulating eIF2α levels may be a viable strategy in the treatment of neurodegenerative diseases. Here, using two genetic approaches, a systemic Gadd34 knockout and a photoreceptor conditional Perk knockout, to alter p-eIF2α levels in rd16 mice, we demonstrate not only that degenerating retinas may not use this mechanism to signal for a decline in protein synthesis rates but also that modulation of p-eIF2α levels is insufficient to delay retinal degeneration.
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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.