Evidence map›Paper›PMID 26798412›Full record

ArticleOxidative medicine and cellular longevity2016

Diabetes-Induced Oxidative Stress in Endothelial Progenitor Cells May Be Sustained by a Positive Feedback Loop Involving High Mobility Group Box-1.

Han Wu, Ran Li, Zhong-Hai Wei, Xin-Lin Zhang, Jian-Zhou Chen, Qing Dai, Jun Xie, Biao Xu

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Han WuDepartment of Cardiology, Drown Tower Hospital, Nanjing University Medical School, Nanjing 210008, China.
Ran LiDepartment of Cardiology, Drown Tower Hospital, Nanjing University Medical School, Nanjing 210008, China.
Zhong-Hai WeiDepartment of Cardiology, Drown Tower Hospital, Nanjing University Medical School, Nanjing 210008, China.
Xin-Lin ZhangDepartment of Cardiology, Drown Tower Hospital, Nanjing University Medical School, Nanjing 210008, China.
Jian-Zhou ChenDepartment of Cardiology, Drown Tower Hospital, Nanjing University Medical School, Nanjing 210008, China.
Qing DaiDepartment of Cardiology, Drown Tower Hospital, Nanjing University Medical School, Nanjing 210008, China.
Jun XieDepartment of Cardiology, Drown Tower Hospital, Nanjing University Medical School, Nanjing 210008, China.
Biao XuDepartment of Cardiology, Drown Tower Hospital, Nanjing University Medical School, Nanjing 210008, China.
Nanjing Drum Tower Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress is considered to be a critical factor in diabetes-induced endothelial progenitor cell (EPC) dysfunction, although the underlying mechanisms are not fully understood. In this study, we investigated the role of high mobility group box-1 (HMGB-1) in diabetes-induced oxidative stress. HMGB-1 was upregulated in both serum and bone marrow-derived monocytes from diabetic mice compared with control mice. In vitro, advanced glycation end productions (AGEs) induced, expression of HMGB-1 in EPCs and in cell culture supernatants in a dose-dependent manner. However, inhibition of oxidative stress with N-acetylcysteine (NAC) partially inhibited the induction of HMGB-1 induced by AGEs. Furthermore, p66shc expression in EPCs induced by AGEs was abrogated by incubation with glycyrrhizin (Gly), while increased superoxide dismutase (SOD) activity in cell culture supernatants was observed in the Gly treated group. Thus, HMGB-1 may play an important role in diabetes-induced oxidative stress in EPCs via a positive feedback loop involving the AGE/reactive oxygen species/HMGB-1 pathway.

Indexed as

Feedback, PhysiologicalOxidative StressAcetylcysteineAnimalsBlood GlucoseBody WeightBone Marrow CellsCells, CulturedDiabetes Mellitus, ExperimentalEndothelial Progenitor CellsGlycation End Products, AdvancedGlycyrrhizic AcidHMGB1 ProteinMaleMice, Inbred C57BLModels, BiologicalAcetylcysteineBlood GlucoseGlycation End Products, AdvancedGlycyrrhizic AcidHMGB1 ProteinShc1 protein, mouseShc Signaling Adaptor ProteinsSrc Homology 2 Domain-Containing, Transforming Protein 1

Identifiers

PMID26798412
PMCPMC4698939
OpenAlexW2261396116

What OpenQuestion holds

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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.