Evidence map›Paper›PMID 35599279›Full record

ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2022

Role of the JAK/STAT pathway in a streptozotocin-induced diabetic retinopathy mouse model.

Chan-Ho Cho, Kug-Hwan Roh, Na-Young Lim, Sung Jae Park, SaeGwang Park, Hyun Woong Kim

Abstract read
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In one paragraph

Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

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  13. TGF-β Signaling Pathways in the Development of Diabetic Retinopathy.International journal of molecular sciences · 2024
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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

6 authors at 2 institutions in 1 country.

Chan-Ho Cho *Department of Ophthalmology, Haeundae Paik Hospital, Inje University College of Medicine, Busan, 48108, Korea.
Kug-Hwan Roh *Department of Microbiology and Immunology, Inje University College of Medicine, Busan, 47392, Korea.
Na-Young LimR&D Center, NexThera Co., Ltd, Busan, 47392, Korea.
Sung Jae ParkDepartment of Internal Medicine, Busan Paik Hospital, Inje University College of Medicine, Busan, 47392, Korea.
SaeGwang ParkDepartment of Microbiology and Immunology, Inje University College of Medicine, Busan, 47392, Korea.
Hyun Woong KimDepartment of Ophthalmology, Haeundae Paik Hospital, Inje University College of Medicine, Busan, 48108, Korea. maekbak9@naver.com.
Inje University · KRInje University Haeundae Paik Hospital · KR

Funding

Ministry of Education NRF-2017R1D1A1B03033799
6 · The paper itself

Abstract

purposeThe Janus tyrosine kinase and signal transducers and activators of transcription (JAK/STAT) pathway is involved in vascular endothelial growth factor (VEGF) expression, but the role of this pathway in diabetic retinopathy (DR) remains unclear. We investigated the role of the JAK/STAT pathway on DR and VEGF expression using a streptozotocin (STZ)-induced DR mouse model.

methodsCultured ARPE-19 cells were exposed to high-glucose conditions and treated with JAK/STAT inhibitors (JAK inhibitor I [JAKiI], tofacitinib, STAT3 inhibitor [STAT3i]) for 48 h. Reverse-transcription polymerase chain reaction, western blotting, and enzyme-linked immunosorbent assay were used to investigate p-JAK/STAT and VEGF expression. Diabetes was induced by intraperitoneal injection of STZ (50 mg/kg) in C57BL/6 mice for 5 days. DR development was evaluated every 4 weeks. JAK/STAT inhibitors were administered for 8 weeks. Immunofluorescence was used to measure the activation status of the JAK/STAT pathway and VEGF production in the retinal tissue.

resultsIn ARPE-19 cells exposed to high-glucose conditions, the mRNA and secretory protein levels of VEGF, p-JAK1, p-JAK2, p-STAT3, and p-STAT5 levels were significantly increased. Treatment with JAKiI, tofacitinib, and STAT3i significantly suppressed VEGF to basal levels at both the mRNA and secretory levels in vitro. In STZ-induced mice, retinal vascular leakage, p-JAK1, p-JAK2, p-JAK3, p-STAT3, and VEGF were significantly increased after diabetes induction. Diabetes-induced retinal vascular leakage was significantly reduced by treatment with JAKiI and tofacitinib. Increased p-JAK1 and VEGF in STZ-induced mice were significantly reduced by JAKiI (p < 0.05, p < 0.001) and tofacitinib (p < 0.001, respectively).

conclusionJAK1 may be more involved in VEGF production and DR progression in mice than JAK2, JAK3, and STAT3.

Indexed as

Diabetes MellitusDiabetic RetinopathyJanus Kinase InhibitorsAnimalsDisease Models, AnimalGlucoseJanus KinasesMiceMice, Inbred C57BLPhosphorylationRNA, MessengerSignal TransductionSTAT5 Transcription FactorSTAT Transcription FactorsStreptozocinTyrosineGlucoseJanus Kinase InhibitorsJanus KinasesRNA, MessengerSTAT5 Transcription FactorSTAT Transcription FactorsStreptozocinTyrosineVascular Endothelial Growth Factor ADiabetic retinopathyJanus tyrosine kinaseSignal transducers and activators of transcriptionVascular endothelial growth factor

Identifiers

PMID35599279
OpenAlexW4281289678

What OpenQuestion holds

Textmetadata
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.