Evidence map›Paper›PMID 21245960›Full record

ArticleMolecular vision2011

Functional characterization of 58-kilodalton inhibitor of protein kinase in protecting against diabetic retinopathy via the endoplasmic reticulum stress pathway.

Hong Yang, Rong Liu, Zheng Cui, Zhi-Qi Chen, Shu Yan, Han Pei, Bin Li

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
  2. Article
  3. Diabetic retinopathy and Alzheimer's disease: Convergence of the unfolded protein response in neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
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  8. Translation deregulation in human disease.Nature reviews. Molecular cell biology · 2018
    Review
  9. Article
  10. Disruption of Protein Processing in the Endoplasmic Reticulum of DYT1 Knock-in Mice Implicates Novel Pathways in Dystonia Pathogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
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  12. Article
  13. Article
  14. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Hong YangDepartment of Ophthalmology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, People's Republic of China.
Rong Liu
Zheng Cui
Zhi-Qi Chen
Shu Yan
Han Pei
Bin Li
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objective58-kilodalton inhibitor of protein kinase (P58(IPK)) plays an important role in preventing endoplasmic reticulum (ER) stress. It is an interferon-induced kinase that targets the eukaryotic translation initiation factor eukaryotic initiation factor 2 alpha. The aim of this study was to determine the roles of P58(IPK) in protecting against diabetic retinopathy (DR) by inhibiting ER stress-signaling mediators.

methodsA rat diabetic model was established by intraperitoneal injection of streptozotocin. Overexpression of P58(IPK) was achieved by intravitreal injection of purified recombinant adeno-associated virus vector (rAAV2)-P58(IPK) or transfection into rat retinal capillary endothelial cells. Retinal vascular permeability was determined by assessing the Evans Blue retinal leakage. To downregulate the P58(IPK) level in cultured rat retinal capillary endothelial cells, pGIPZ-P58(IPK) RNA interference (P58(IPK)RNAi) was introduced in these cells. Real time reverse transcription (RT)-PCR and western blot analyses were performed to evaluate the mRNA and protein levels of Core/emopamil binding protein (C/EBP) homologous protein (CHOP), vascular endothelial growth factor (VEGF), and tumor necrosis factor-α (TNF-α).

resultsRetinal blood vessel leakage was significantly decreased in rAAV2-P58(IPK)-transfected diabetic rats compared with the control diabetic rats. Both mRNA and protein levels of CHOP, TNF-α, and VEGF in the retina of diabetic rats were remarkably reduced in P58(IPK)-transfected rats. In vitro study further demonstrated that overexpression of P58(IPK) downregulated the expression of CHOP, TNF-α, and VEGF under high glucose conditions, whereas introduction of P58(IPK)RNAi enhanced the expression of CHOP, TNF-α, and VEGF.

conclusionsThese results revealed the protecting role of P58(IPK) against ER stress-mediated DR in diabetic rats, suggesting that P58(IPK) may act as a DR-resistant gene during diabetes.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetic RetinopathyDisease Models, AnimalEndoplasmic ReticulumEukaryotic Initiation Factor-2GlucoseHSP40 Heat-Shock ProteinsMaleOxidative StressProtein KinasesRatsRats, Sprague-DawleyRetinal VesselsRNA InterferenceSignal TransductionDDIT3 protein, humanEukaryotic Initiation Factor-2GlucoseHSP40 Heat-Shock ProteinsProtein KinasesTranscription Factor CHOPTumor Necrosis Factor-alphaVascular Endothelial Growth Factor A

Identifiers

PMID21245960
PMCPMC3021576
OpenAlexW2120613466

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Registered trials

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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.