Evidence map›Paper›PMID 26454330›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2015

HMGB-1 as a Potential Target for the Treatment of Diabetic Retinopathy.

Hailan Zhao, Jingzhuang Zhang, Jie Yu

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  12. Expression of High-Mobility Group Box 1 Protein (HMGB1) and Toll-Like Receptor 9 (TLR9) in Retinas of Diabetic Rats.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  13. [Association between high-mobility group box 1 and neonatal respiratory distress syndrome].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017
    Article
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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

3 authors at 1 institution in 1 country.

Hailan ZhaoDepartment of Ophthalmology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang, China (mainland).
Jingzhuang ZhangDepartment of Ophthalmology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang, China (mainland).
Jie YuDepartment of Ophthalmology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang, China (mainland).
Zhejiang Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic retinopathy (DR) is one of the most important complications of diabetes mellitus (DM) and is the leading cause of blindness in diabetic patients. Recent studies showed that as important inflammatory mediators, high mobility group box 1 (HMGB-1) is associated with diabetic peripheral neuropathy and can participate in the occurrence and development of DR. This study explored HMGB-1 as a therapeutic target for DR treatment through observing its role in retinal ganglion cells (GRCs) in a high glucose environment. MATERIAL AND

methodsRGCs were randomly divided into 3 groups: the normal control group, the high glucose group, and the siRNA HMGB-1 group. Real-time PCR was used to detect HMGB-1 mRNA expression. ELISA was used to test HMGB-1 protein expression in the supernatant. MTT assay was performed to determine cell proliferation. Real-time PCR and Western blotting were used to analyze TLR4 and NF-κB expression.

resultsHMGB-1 mRNA was up-regulated (P=0.015) and protein secretion increased (P=0.022) in the high glucose environment. RGCs survival decreased (P=0.026), while TLR4 and NF-κB mRNA (P=0.009 and P=0.017, respectively) and protein expression increased significantly (P=0.041 and P=0.024, respectively). SiRNA HMGB-1 transfection obviously inhibited HMGB-1 mRNA expression (P=0.032), reduced HMGB-1 secretion (P=0.012), and decreased TLR4 and NF-κB mRNA (P=0.033 and P=0.024, respectively) and protein expression (P=0.032; P=0.027, respectively). Compared with the high glucose group, the RGCs survival rate increased significantly (P=0.037).

conclusionsAs a therapeutic target, HMGB-1 can inhibit inflammation and promote RGCs survival to delay DR progress through the HMGB-1-TLR4-NF-κB signaling pathway.

Indexed as

Blood GlucoseCell LineCell SurvivalDiabetic RetinopathyEnzyme-Linked Immunosorbent AssayHMGB1 ProteinHumansInflammationNF-kappa B p50 SubunitPeripheral Nervous System DiseasesReal-Time Polymerase Chain ReactionRetinal Ganglion CellsRNA, MessengerRNA, Small InterferingTetrazolium SaltsThiazolesBlood GlucoseHMGB1 ProteinHMGB1 protein, humanNF-kappa B p50 SubunitNFKB1 protein, humanRNA, MessengerRNA, Small InterferingTetrazolium SaltsThiazolesthiazolyl blueTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID26454330
PMCPMC4604733
OpenAlexW2216439475

What OpenQuestion holds

Textmetadata
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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.