Evidence map›Paper›PMID 30384259›Full record

ReviewRedox biology2019

New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis.

Ting Yuan, Ting Yang, Huan Chen, Danli Fu, Yangyang Hu, Jing Wang, Qing Yuan, Hong Yu, Wenfeng Xu, Xiang Xie

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 391 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
391citing papers in PubMed, 2 pooled it
33.2field-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

391 citing papers in PubMed, 2 syntheses or guidelines pooled it, 728 citations in OpenAlex.

  1. Pooled it
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  7. Unravelling the Therapeutic Potential of Cysteine for Cardiovascular Health.International journal of molecular sciences · 2026
    Review
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  20. Evaluating the cardio-protective effects ofCardiovascular endocrinology & metabolism · 2026
    Article

331 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

10 authors at 1 institution in 1 country.

Ting YuanThe School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan Province 646000, China.
Ting YangThe School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan Province 646000, China.
Huan ChenThe School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan Province 646000, China. Electronic address: huanchen@swmu.edu.cn.
Danli FuThe School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan Province 646000, China.
Yangyang HuThe School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan Province 646000, China.
Jing WangThe School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan Province 646000, China.
Qing YuanThe School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan Province 646000, China.
Hong YuThe School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan Province 646000, China.
Wenfeng XuThe School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan Province 646000, China.
Xiang XieThe School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan Province 646000, China. Electronic address: xiangxie@swmu.edu.cn.
Southwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress and inflammation interact in the development of diabetic atherosclerosis. Intracellular hyperglycemia promotes production of mitochondrial reactive oxygen species (ROS), increased formation of intracellular advanced glycation end-products, activation of protein kinase C, and increased polyol pathway flux. ROS directly increase the expression of inflammatory and adhesion factors, formation of oxidized-low density lipoprotein, and insulin resistance. They activate the ubiquitin pathway, inhibit the activation of AMP-protein kinase and adiponectin, decrease endothelial nitric oxide synthase activity, all of which accelerate atherosclerosis. Changes in the composition of the gut microbiota and changes in microRNA expression that influence the regulation of target genes that occur in diabetes interact with increased ROS and inflammation to promote atherosclerosis. This review highlights the consequences of the sustained increase of ROS production and inflammation that influence the acceleration of atherosclerosis by diabetes. The potential contributions of changes in the gut microbiota and microRNA expression are discussed.

Indexed as

Diabetes ComplicationsOxidative StressAnimalsAtherosclerosisGastrointestinal MicrobiomeGlycation End Products, AdvancedHumansHyperglycemiaInflammationInsulin ResistanceIntracellular SpaceMicroRNAsMitochondriaProtein Kinase CReactive Oxygen SpeciesSignal TransductionGlycation End Products, AdvancedMicroRNAsProtein Kinase CReactive Oxygen SpeciesAtherosclerosisDiabetes mellitusGut microbiotaMicroRNAReactive oxygen species

Identifiers

PMID30384259
PMCPMC6205410
OpenAlexW2897364906

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.