Evidence map›Paper›PMID 32901881›Full record

ArticleMolecular medicine reports2020

ITCH regulates oxidative stress induced by high glucose through thioredoxin interacting protein in cultured human lens epithelial cells.

Lingfeng Jiang, Wenkai Zhou, Bo Lu, Qichang Yan

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Loss of Peroxiredoxin 6 Drives Age-Related Klf9/NF-Antioxidants (Basel, Switzerland) · 2026
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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

4 authors at 2 institutions in 1 country.

Lingfeng JiangDepartment of Ophthalmology, Fourth Affiliated Hospital of China Medical University, Ophthalmology Hospital of China Medical University, Key Laboratory of Lens in Liaoning Province, Shenyang, Liaoning 110005, P.R. China.
Wenkai ZhouDepartment of Ophthalmology, Fourth Affiliated Hospital of China Medical University, Ophthalmology Hospital of China Medical University, Key Laboratory of Lens in Liaoning Province, Shenyang, Liaoning 110005, P.R. China.
Bo LuDepartment of Ophthalmology, Fourth Affiliated Hospital of China Medical University, Ophthalmology Hospital of China Medical University, Key Laboratory of Lens in Liaoning Province, Shenyang, Liaoning 110005, P.R. China.
Qichang YanDepartment of Ophthalmology, Fourth Affiliated Hospital of China Medical University, Ophthalmology Hospital of China Medical University, Key Laboratory of Lens in Liaoning Province, Shenyang, Liaoning 110005, P.R. China.
China Medical University · CNFourth Affiliated Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thioredoxin (Trx) is an important protein that controls oxidative damage in almost all eukaryotic cells. Trx interaction protein (Txnip) has been reported to negatively regulate the bioavailability of Trx and inhibit its biological function. The E3 ubiquitin ligase ITCH can specifically degrade Txnip via ubiquitination. The apoptosis of human lens epithelial cells (HLECs), which are highly sensitive to redox caused by oxidative stress, is a significant factor for the development of sugar cataract in a high‑glucose environment. However, whether Trx, Txnip and ITCH contribute to the progression of sugar cataracts and the underlying mechanisms remain unknown, and thus, identifying these were the aims of the present study. The present results suggested that the expression levels of Trx, Txnip and ITCH in HLECs cultured with different glucose concentrations were detected by reverse transcription‑quantitative PCR and western blotting, and the apoptotic rate of the cells was detected by flow cytometry and superoxide detection assay. The interaction between ITCH and Txnip was determined by co‑localization immunofluorescence and co‑immunoprecipitation. In addition, a vector and small interfering RNA of ITCH were transfected to overexpress and knockdown ITCH, respectively, to alter the expression of downstream proteins and cell apoptosis. It was found that Txnip was highly expressed in cultured HLECs in high‑glucose environment, and the antioxidative function of Trx was restricted and suppressed, thus promoting apoptosis. The overexpression of ITCH increased the expression of Trx and decreased oxidative stress and apoptosis by decreasing Txnip in cultured HLECs, while downregulation of ITCH significantly decreased the expression of Trx and enhanced oxidative stress and apoptosis. Therefore, the present results indicated that ITCH could regulate the apoptosis of HLECs that were cultured in high‑glucose concentration and that it may be a treatment target for sugar cataract.

Indexed as

ApoptosisCarrier ProteinsCell Culture TechniquesCell LineEpithelial CellsGlucoseHumansLens, CrystallineOxidative StressProteolysisRepressor ProteinsThioredoxinsUbiquitinationUbiquitin-Protein LigasesUp-RegulationCarrier ProteinsGlucoseITCH protein, humanRepressor ProteinsThioredoxinsTXNIP protein, humanTXN protein, humanUbiquitin-Protein Ligases

Identifiers

PMID32901881
PMCPMC7533507
OpenAlexW3084124382

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.