Evidence map›Paper›PMID 31432194›Full record

ArticleMolecular medicine reports2019

Accumulation of advanced glycation end products potentiate human retinal capillary endothelial cells mediated diabetic retinopathy.

Dan Tao, Ninghua Ni, Tiesong Zhang, Chao Li, Qing Sun, Ling Wang, Yan Mei

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Bibliometric analysis and visualization of inflammation in the field of diabetic retinopathy research (2006-2025).Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026
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  18. The role of RAGE in host pathology and crosstalk between RAGE and TLR4 in innate immune signal transduction pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Review
  19. Endothelial Dysfunction in Diabetic Retinopathy.Frontiers in endocrinology · 2020
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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 3 institutions in 1 country.

Dan TaoCollege of Environmental Science and Engineering, Kunming University of Science and Technology, Kunming, Yunnan 650500, P.R. China.
Ninghua NiDepartment of Ophthalmology, The First People's Hospital of Yunnan Province, Kunming, Yunnan 650031, P.R. China.
Tiesong ZhangDepartment of Otolaryngology, Kunming Children's Hospital, Kunming, Yunnan 650228, P.R. China.
Chao LiDepartment of Anesthesiology, Kunming Children's Hospital, Kunming, Yunnan 650228, P.R. China.
Qing SunDepartment of Ophthalmology, Kunming Children's Hospital, Kunming, Yunnan 650031, P.R. China.
Ling WangDepartment of Ophthalmology, Kunming Children's Hospital, Kunming, Yunnan 650031, P.R. China.
Yan MeiSchool of Medicine, Kunming University of Science and Technology, Kunming, Yunnan 650500, P.R. China.
Kunming Children's Hospital · CNKunming University of Science and Technology · CNFirst People's Hospital of Yunnan Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The major ophthalmic complication in patients with diabetes is diabetic retinopathy (DR), which is one of the major eye diseases that causes blindness. It is well established that the occurrence and duration of DR is positively correlated with duration of diabetes. Advanced glycation end product (AGE) accumulation in patients with diabetes is one factor that leads to the development of DR. However, the underlying mechanisms remain unclear. In the present study, the role of phosphoinositide 3‑kinase/protein kinase B (Akt) signaling in AGE‑induced DR development was investigated. An in vitro experimental system was used to study the effects of AGEs on human retinal capillary endothelial cells (HRCECs) and Müller cells. Flow cytometry, MTT, western blotting and BrdU incorporation assays were performed. Reverse transcription‑quantitative polymerase chain reaction was used to measure the expression of angiogenesis‑associated genes. Functional assays of angiogenesis, including HRCEC invasion and tube formation assays. It was demonstrated that the expression of receptor for AGEs was upregulated in HRCECs and Müller cells following treatment with AGEs. AGE treatment did not affect Müller cell viability, but enhanced HRCEC viability. Akt inhibition increased cell apoptosis and death in HRCECs. AGE treatment upregulated the expression of pro‑angiogenic genes, which was suppressed by Akt inhibitor treatment. In addition, Akt inhibitor treatment suppressed HRCEC invasion and tube formation ability. The present study suggested that Akt‑mediated signaling may serve critical roles in the development of DR due to the accumulation of AGEs. Akt may be a potential therapeutic target in DR.

Indexed as

ApoptosisCell LineDiabetic RetinopathyEndothelial CellsGlycation End Products, AdvancedHumansNeovascularization, PathologicRetinaRetinal VesselsGlycation End Products, Advanced

Identifiers

PMID31432194
PMCPMC6755164
OpenAlexW2969917976

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.