Evidence map›Paper›PMID 28427390›Full record

ArticleCardiovascular diabetology2017

Advanced glycation end-products decreases expression of endothelial nitric oxide synthase through oxidative stress in human coronary artery endothelial cells.

Xiaomei Ren, Liqun Ren, Qin Wei, Hua Shao, Long Chen, Naifeng Liu

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
9.4field-weighted citation impact, top 1% 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

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.

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  13. Decoding Vascular Senescence: Cellular Insights and Therapeutic Strategies.International journal of biological sciences · 2026
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44 more citing papers are in PubMed but not listed here.

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.

Xiaomei RenDepartment of Geriatrics, Zhongda Hospital, School of Medicine, Southeast University, No. 87, Dingjiaqiao Road, Nanjing, 210009, China.
Liqun RenDepartment of Geriatrics, Zhongda Hospital, School of Medicine, Southeast University, No. 87, Dingjiaqiao Road, Nanjing, 210009, China.
Qin WeiDepartment of Cardiology, Zhongda Hospital, School of Medicine, Southeast University, No. 87, Dingjiaqiao Road, Nanjing, 210009, China. WeiQin1102@163.com.
Hua ShaoDepartment of Pharmacy, Zhongda Hospital, Southeast University, No. 87, Dingjiaqiao Road, Nanjing, 210009, China.
Long ChenDepartment of Cardiology, Zhongda Hospital, School of Medicine, Southeast University, No. 87, Dingjiaqiao Road, Nanjing, 210009, China.
Naifeng LiuSchool of Medicine, Southeast University, No. 87, Dingjiaqiao Road, Nanjing, 210009, China.
Zhongda Hospital Southeast University · CNSoutheast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdvanced glycation end-products (AGEs) are elevated under diabetic conditions and associated with insulin resistance, endothelial dysfunction and vascular inflammation in humans. It has been demonstrated that AGEs evoke oxidative and inflammatory reactions in endothelial cells through the interaction with a receptor for AGEs (RAGE). Here, we aimed to identify the cellular mechanisms by which AGEs exacerbate the endothelial dysfunction in human coronary artery endothelial cells (HCAECs).

methods30 type 2 diabetic patients with or without coronary artery atherosclerosis were recruited for this study. Plasma levels of AGE peptides (AGE-p) were analyzed using flow injection assay. Endothelial function was tested by brachial artery flow-mediated vasodilatation (FMD). Further investigations were performed to determine the effects and mechanisms of AGEs on endothelial dysfunction in HCAECs.

resultsAGE-p was inversely associated with FMD in diabetic patients with coronary artery atherosclerosis in our study. After treated with AGEs, HCAECs showed significant reductions of eNOS mRNA and protein levels including eNOS and phospho-eNOS Ser1177, eNOS mRNA stability, eNOS enzyme activity, and cellular nitric oxide (NO) levels, whereas superoxide anion production was significantly increased. In addition, AGEs significantly decreased mitochondrial membrane potential, ATP content and catalase and superoxyde dismutase (SOD) activities, whereas it increased NADPH oxidase activity. Treatment of the cells with antioxidants SeMet, SOD mimetic MnTBAP and mitochondrial inhibitor thenoyltrifluoroacetone (TTFA) effectively blocked these effects induced by AGEs. AGEs also increased phosphorylation of the mitogen-activated protein kinases p38 and ERK1/2, whereas the specific inhibitors of p38, ERK1/2, and TTFA effectively blocked AGEs-induced reactive oxygen species production and eNOS downregulation.

conclusionsAGEs cause endothelial dysfunction by a mechanism associated with decreased eNOS expression and increased oxidative stress in HCAECs through activation of p38 and ERK1/2.

Indexed as

Gene Expression Regulation, EnzymologicAdultAgedCells, CulturedCoronary VesselsDose-Response Relationship, DrugEndothelial CellsEndothelium, VascularFemaleGlycation End Products, AdvancedHumansMaleMiddle AgedNitric Oxide Synthase Type IIIOxidative StressGlycation End Products, AdvancedNitric Oxide Synthase Type IIINOS3 protein, humanAdvanced glycation end-productsEndothelial dysfunctionEndothelial nitric oxide synthaseOxidative stress

Identifiers

PMID28427390
PMCPMC5397770
OpenAlexW2605434555

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.