Evidence map›Paper›PMID 32103904›Full record

ArticleDrug design, development and therapy2020

Hydrogen Sulfide Protects Against High Glucose-Induced Human Umbilical Vein Endothelial Cell Injury Through Activating PI3K/Akt/eNOS Pathway.

Fengxia Lin, Yiying Yang, Shanyin Wei, Xiaojing Huang, Zhijian Peng, Xiao Ke, Zhicong Zeng, Yinzhi Song

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 117 citations in OpenAlex.

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11 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

8 authors at 3 institutions in 1 country.

Fengxia Lin *Department of Cardiology, Shenzhen Bao'an Traditional Chinese Medicine Hospital Group, The Affiliated Hospital of Guangzhou University of Chinese Medicine, Shenzhen 518133, People's Republic of China.
Yiying Yang *Department of Cardiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, People's Republic of China.
Shanyin WeiDepartment of Cardiology, Shenzhen Bao'an Traditional Chinese Medicine Hospital Group, The Affiliated Hospital of Guangzhou University of Chinese Medicine, Shenzhen 518133, People's Republic of China.
Xiaojing HuangDepartment of Cardiology, Shenzhen Bao'an Traditional Chinese Medicine Hospital Group, The Affiliated Hospital of Guangzhou University of Chinese Medicine, Shenzhen 518133, People's Republic of China.
Zhijian PengDepartment of Cardiology, Shenzhen Bao'an Traditional Chinese Medicine Hospital Group, The Affiliated Hospital of Guangzhou University of Chinese Medicine, Shenzhen 518133, People's Republic of China.
Xiao KeDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, (Shenzhen Sun Yat-sen Cardiovascular Hospital), Shenzhen 518057, People's Republic of China.
Zhicong ZengDepartment of Cardiology, Shenzhen Bao'an Traditional Chinese Medicine Hospital Group, The Affiliated Hospital of Guangzhou University of Chinese Medicine, Shenzhen 518133, People's Republic of China.
Yinzhi SongDepartment of Cardiology, Shenzhen Bao'an Traditional Chinese Medicine Hospital Group, The Affiliated Hospital of Guangzhou University of Chinese Medicine, Shenzhen 518133, People's Republic of China.
Guangzhou University of Chinese Medicine · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeDysfunction of endothelial cells plays a key role in the pathogenesis of diabetic atherosclerosis. High glucose (HG) has been found as a key factor in the progression of diabetic complications, including atherosclerosis. PI3K/Akt/eNOS signaling pathway has been shown to involve in HG-induced vascular injuries. Hydrogen sulfide (H MATERIALS AND

methodsThe endothelial protective effects of H

resultsHG treatment significantly inhibited PI3K/Akt/eNOS signaling in HUVECs, which was partially reversed by the H2S treatment. HG treatment inhibited cell viability of HUVECs, which were markedly prevented by H

conclusionThe present study demonstrated that exogenous H

Indexed as

ApoptosisAtherosclerosisCell SurvivalDiabetes ComplicationsDisease ProgressionGlucoseHumansHuman Umbilical Vein Endothelial CellsHydrogen SulfideNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinaseProtective AgentsProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSignal TransductionGlucoseHydrogen SulfideNitric Oxide Synthase Type IIINOS3 protein, humanPhosphatidylinositol 3-KinaseProtective AgentsProto-Oncogene Proteins c-aktReactive Oxygen Speciesendothelial cellshigh glucosehydrogen sulfideinjuryPI3K/Akt/eNOS

Identifiers

PMID32103904
PMCPMC7027865
OpenAlexW3006078128

What OpenQuestion holds

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LicenceCC BY-NC
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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.