Evidence map›Paper›PMID 33162888›Full record

ArticleFrontiers in pharmacology2020

Metformin Ameliorates Gestational Diabetes Mellitus-Induced Endothelial Dysfunction

Cong Cong Sun, Ya Nan Lai, Wen Huan Wang, Xiao Min Xu, Xiao Qing Li, Hai Wang, Jia Yong Zheng, Jian Qiong Zheng

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 32 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.

Cong Cong SunWenzhou Key Laboratory of Obstetrics and Gynecology, The Third Affiliated Clinical Institute of Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospital, Wenzhou, China.
Ya Nan LaiWenzhou Key Laboratory of Obstetrics and Gynecology, The Third Affiliated Clinical Institute of Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospital, Wenzhou, China.
Wen Huan WangWenzhou Key Laboratory of Obstetrics and Gynecology, The Third Affiliated Clinical Institute of Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospital, Wenzhou, China.
Xiao Min XuWenzhou Key Laboratory of Obstetrics and Gynecology, The Third Affiliated Clinical Institute of Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospital, Wenzhou, China.
Xiao Qing LiWenzhou Key Laboratory of Obstetrics and Gynecology, The Third Affiliated Clinical Institute of Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospital, Wenzhou, China.
Hai WangWenzhou Key Laboratory of Obstetrics and Gynecology, The Third Affiliated Clinical Institute of Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospital, Wenzhou, China.
Jia Yong ZhengWenzhou Key Laboratory of Obstetrics and Gynecology, The Third Affiliated Clinical Institute of Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospital, Wenzhou, China.
Jian Qiong ZhengDepartment of Obstetrics and Gynecology, The Third Affiliated Clinical Institute of Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou Maternal and Child Health Care Hospital, Wenzhou, China.
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gestational diabetes mellitus (GDM) causes oxidative stress in mothers and infants and causes vascular endothelial dysfunction, which is a key factor for maternal and fetal cardiovascular diseases in the later stage of GDM, seriously threatening the life and health of mothers and infants. Nowadays, metformin (MET) has been discovered to improve endothelial function, but studies regarding the mechanism of MET improving endothelial cell function and alleviating endothelial function under hyperglycemia are still extremely limited. We aimed to investigate whether MET exerts its protective role against hyperglycemia-induced endothelial dysfunction through p65 and Nrf2. In our studies, applying cell migration assay and tube formation assay, we observed an obvious improvement of endothelial function under MET-treated, as characterized by that MET accelerated GDM-attenuated migration and angiogenesis of HUVECs. And ELISA assay results uncovered that Nrf2 expression level was decreased in GDM placenta, HVUECs and maternal serum comparing with normal group, however activation Nrf2 largely ameliorated tube formation under hyperglycemic condition. Furthermore, MET elevated the Nrf2 expression level and the level of nuclear Nrf2 accumulation in hyperglycemic HUVECs. Besides, preliminary evidence predicted that Nrf2 expression was modulated by transcription factor p65, which was increased in GDM peripheral blood, placenta and HUVECs, and suppression of p65 could recover GDM-induced suppression of angiogenesis. In addition, we also confirmed MET restores the GDM-induced angiogenesis impairment may

Indexed as

endothelial dysfunctiongestational diabetes mellitusmetforminNrf2p65

Identifiers

PMID33162888
PMCPMC7581851
OpenAlexW3092115102

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.