Evidence map›Paper›PMID 27635402›Full record

ArticleJournal of diabetes research2016

High Glucose-Induced Oxidative Stress Mediates Apoptosis and Extracellular Matrix Metabolic Imbalances Possibly via p38 MAPK Activation in Rat Nucleus Pulposus Cells.

Xiaofei Cheng, Bin Ni, Feng Zhang, Ying Hu, Jie Zhao

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.1field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. PI3KCD gene expression and its role in diabetic intervertebral disc degeneration running title: PI3KCD gene crucial for diabetic IDH.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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  15. The Proteolysis of ECM in Intervertebral Disc Degeneration.International journal of molecular sciences · 2022
    Review
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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

5 authors at 3 institutions in 1 country.

Xiaofei ChengShanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedic Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhizaoju Road, Shanghai 200011, China.
Bin NiDepartment of Orthopedics, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Feng ZhangShanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedic Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhizaoju Road, Shanghai 200011, China.
Ying HuDepartment of Toxicity Evaluation, Shanghai Municipal Center for Disease Control and Prevention, Shanghai, China.
Jie ZhaoShanghai Key Laboratory of Orthopaedic Implants, Department of Orthopaedic Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhizaoju Road, Shanghai 200011, China.ORCID 0000-0002-4504-8193
Shanghai Jiao Tong University · CNSecond Military Medical University · CNShanghai Municipal Center For Disease Control Prevention · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives. To investigate whether high glucose-induced oxidative stress is implicated in apoptosis of rat nucleus pulposus cells (NPCs) and abnormal expression of critical genes involved in the metabolic balance of extracellular matrix (ECM). Methods. NPCs were cultured with various concentrations of glucose to detect cell viability and apoptosis. Cells cultured with high glucose (25 mM) were untreated or pretreated with N-acetylcysteine or a p38 MAPK inhibitor SB 202190. Reactive oxygen species (ROS) production was evaluated. Activation of p38 MAPK was measured by Western blot. The expression of ECM metabolism-related genes, including type II collagen, aggrecan, SRY-related high-mobility-group box 9 (Sox-9), matrix metalloproteinase 3 (MMP-3), and tissue inhibitor of metalloproteinase 1 (TIMP-1), was analyzed by semiquantitative RT-PCR. Results. High glucose reduced viability of NPCs and induced apoptosis. High glucose resulted in increased ROS generation and p38 MAPK activation. In addition, it negatively regulated the expression of type II collagen, aggrecan, Sox-9, and TIMP-1 and positively regulated MMP-3 expression. These results were changed by pretreatment with N-acetylcysteine or SB 202190. Conclusions. High glucose might promote apoptosis of NPCs, trigger ECM catabolic pathways, and inhibit its anabolic activities, possibly through a p38 MAPK-dependent oxidative stress mechanism.

Indexed as

AcetylcysteineAggrecansAnimalsApoptosisBlotting, WesternCells, CulturedCell SurvivalCollagen Type IIExtracellular MatrixFree Radical ScavengersGlucoseHumansHyperglycemiaMatrix Metalloproteinase 3Nucleus PulposusOxidative StressAcetylcysteineAggrecansCollagen Type IIFree Radical ScavengersGlucoseMatrix Metalloproteinase 3p38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesRNA, MessengerSOX9 Transcription FactorTIMP1 protein, ratTissue Inhibitor of Metalloproteinase-1

Identifiers

PMID27635402
PMCPMC5011214
OpenAlexW2513703929

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Registered trials

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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.