Evidence map›Paper›PMID 36756695›Full record

ArticleJournal of diabetes investigation2023

BASP1 promotes high glucose-induced endothelial apoptosis in diabetes via activation of EGFR signaling.

Fengnan Sun, Junwei Liu, Yanzheng Wang, Hongmei Yang, Danfeng Song, Haiyan Fu, Xingxing Feng

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

6 citing papers in PubMed, 10 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

7 authors at 2 institutions in 1 country.

Fengnan SunDepartment of Laboratory Medicine, Yantaishan Hospital, Yantai, China.
Junwei LiuDepartment of Laboratory Medicine, Qishan Hospital, Yantai, China.
Yanzheng WangDepartment of Laboratory Medicine, Yantaishan Hospital, Yantai, China.
Hongmei YangDepartment of Laboratory Medicine, Yantaishan Hospital, Yantai, China.
Danfeng SongDepartment of Laboratory Medicine, Yantaishan Hospital, Yantai, China.
Haiyan FuDepartment of Laboratory Medicine, Yantaishan Hospital, Yantai, China.
Xingxing FengKunming Key Laboratory of Children Infection and Immunity, Yunnan Key Laboratory of Children's Major Disease Research, Yunnan Institute of Pediatrics, Kunming Children's Hospital, Kunming, China.ORCID https://orcid.org/0000-0003-1673-8491
Yantaishan Hospital · CNKunming Children's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsDiabetes mellitus is a common chronic disease of glucose metabolism. Endothelial dysfunction is an early event in diabetes complicated by cardiovascular disease. This study aimed to reveal the expression of BASP1 and its biological roles in endothelial cell dysfunction in diabetes complicated by cardiovascular disease. MATERIALS AND

methodsBy analyzing the databases related to diabetes complicated with coronary heart disease, BASP1 was screened out as an upregulated gene. Human umbilical vein endothelial cells (HUVECs) and primary mouse aortic endothelial cells were treated with high glucose to establish cell models of diabetes-related endothelial dysfunction, and the expression changes of BASP1 were verified by RT-qPCR, western blot, and immunofluorescence. BASP1 was silenced or overexpressed by siRNA or overexpression plasmid, and its effects on cell migration, apoptosis, tube formation, inflammatory response, and ROS were detected. The possible signaling pathway of BASP1 was found and the mechanism of BASP1 on promoting the progression of endothelial dysfunction was explored using the EGFR inhibitor, gefitinib.

resultsBioinformatics analysis indicated that the expression of BASP1 in patients with diabetes mellitus and concomitant coronary heart disease was increased. High glucose induced the upregulation of BASP1 expression in endothelial cells, and showed a time-dependent relationship. Silencing of BASP1 alleviated the damage of high glucose to endothelial cells. BASP1 regulated EGFR positively. The promoting effect of BASP1 on endothelial cell apoptosis may be achieved by regulating the EGFR pathway.

conclusionBASP1 promotes endothelial cell injury induced by high glucose in patients with diabetes, which may be activated by activating the EGFR pathway.

Indexed as

Cardiovascular DiseasesDiabetes MellitusAnimalsApoptosisCalmodulin-Binding ProteinsCytoskeletal ProteinsErbB ReceptorsGlucoseHumansHuman Umbilical Vein Endothelial CellsMembrane ProteinsMiceNerve Tissue ProteinsRepressor ProteinsSignal TransductionBASP1 protein, humanBasp1 protein, mouseCalmodulin-Binding ProteinsCytoskeletal ProteinsEGFR protein, humanErbB ReceptorsGlucoseMembrane ProteinsNerve Tissue ProteinsRepressor ProteinsBASP1DiabetesEGFR

Identifiers

PMID36756695
PMCPMC10034959
OpenAlexW4319656535

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.