Evidence map›Paper›PMID 33594332›Full record

ArticleWorld journal of diabetes2021

Role of ferroptosis in the process of diabetes-induced endothelial dysfunction.

Er-Fei Luo, Hong-Xia Li, Yu-Han Qin, Yong Qiao, Gao-Liang Yan, Yu-Yu Yao, Lin-Qing Li, Jian-Tong Hou, Cheng-Chun Tang, Dong Wang

Open access · diamondAbstract read
In one paragraph

Article in World journal of diabetes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 2 pooled it
15.6field-weighted citation impact, top 1% 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

93 citing papers in PubMed, 2 syntheses or guidelines pooled it, 134 citations in OpenAlex.

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33 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

10 authors at 1 institution in 1 country.

Er-Fei LuoSchool of Medicine, Southeast University, Nanjing 210009, Jiangsu Province, China.
Hong-Xia LiSchool of Medicine, Southeast University, Nanjing 210009, Jiangsu Province, China.
Yu-Han QinSchool of Medicine, Southeast University, Nanjing 210009, Jiangsu Province, China.
Yong QiaoDepartment of Cardiology, Zhongda Hospital, Southeast University, Nanjing 210009, Jiangsu Province, China.
Gao-Liang YanDepartment of Cardiology, Zhongda Hospital, Southeast University, Nanjing 210009, Jiangsu Province, China.
Yu-Yu YaoDepartment of Cardiology, Zhongda Hospital, Southeast University, Nanjing 210009, Jiangsu Province, China.
Lin-Qing LiSchool of Medicine, Southeast University, Nanjing 210009, Jiangsu Province, China.
Jian-Tong HouDepartment of Cardiology, Zhongda Hospital, Southeast University, Nanjing 210009, Jiangsu Province, China.
Cheng-Chun TangDepartment of Cardiology, Zhongda Hospital, Southeast University, Nanjing 210009, Jiangsu Province, China.
Dong WangDepartment of Cardiology, Zhongda Hospital, Southeast University, Nanjing 210009, Jiangsu Province, China. wangdong_seu@163.com.
Southeast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndothelial dysfunction, a hallmark of diabetes, is a critical and initiating contributor to the pathogenesis of diabetic cardiovascular complications. However, the underlying mechanisms are still not fully understood. Ferroptosis is a newly defined regulated cell death driven by cellular metabolism and iron-dependent lipid peroxidation. Although the involvement of ferroptosis in disease pathogenesis has been shown in cancers and degenerative diseases, the participation of ferroptosis in the pathogenesis of diabetic endothelial dysfunction remains unclear.

aimTo examine the role of ferroptosis in diabetes-induced endothelial dysfunction and the underlying mechanisms.

methodsHuman umbilical vein endothelial cells (HUVECs) were treated with high glucose (HG), interleukin-1β (IL-1β), and ferroptosis inhibitor, and then the cell viability, reactive oxygen species (ROS), and ferroptosis-related marker protein were tested. To further determine whether the p53-xCT (the substrate-specific subunit of system Xc

resultsIt was found that HG and IL-1β induced ferroptosis in HUVECs, as evidenced by the protective effect of the ferroptosis inhibitors, Deferoxamine and ferrostatin-1, resulting in increased lipid ROS and decreased cell viability. Mechanistically, activation of the p53-xCT-GSH axis induced by HG and IL-1β enhanced ferroptosis in HUVECs. In addition, a decrease in xCT and the presence of de-endothelialized areas were observed in the aortic endothelium of db/db mice.

conclusionFerroptosis is involved in endothelial dysfunction and p53-xCT-GSH axis activation plays a crucial role in endothelial cell ferroptosis and endothelial dysfunction.

Indexed as

Diabetes mellitusEndothelial dysfunctionFerroptosisGlutathionep53Reactive oxygen species

Identifiers

PMID33594332
PMCPMC7839168
OpenAlexW3124597957

What OpenQuestion holds

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LicenceCC BY-NC
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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.