Evidence map›Paper›PMID 38702777›Full record

ArticleCardiovascular diabetology2024

Ion channel Piezo1 activation aggravates the endothelial dysfunction under a high glucose environment.

Xiaoyu Zhang, Shaoqiu Leng, Xinyue Liu, Xiang Hu, Yan Liu, Xin Li, Qi Feng, Wei Guo, Nailin Li, Zi Sheng and 2 more

Abstract read
In one paragraph

Article in Cardiovascular diabetology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

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  15. Piezo1 disrupts blood-brain barrier via CaMKII/Nrf2 in ischemic stroke.Cellular and molecular life sciences : CMLS · 2025
    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

12 authors.

Xiaoyu Zhang *Department of Hematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Shaoqiu Leng *Department of Hematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Xinyue LiuDepartment of Hematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Xiang HuAdvanced Medical Research Institute, Shandong University, Jinan, China.
Yan LiuDepartment of Hematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Xin LiDepartment of Hematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Qi FengDepartment of Hematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Wei GuoInstitute of Hematology, the First Affiliated Hospital of Zhejiang University School of Medicine, Zhejiang University, Hangzhou, 310029, China.
Nailin LiDepartment of Medicine-Solna, Cardiovascular Medicine Unit, Karolinska Institutet, Stockholm, Sweden.
Zi ShengShandong Key Laboratory of Immunochematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Shuwen WangShandong Key Laboratory of Immunochematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China. 15066693988@163.com.
Jun PengDepartment of Hematology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China. junpeng88@sina.com.cn.ORCID 0000-0003-1434-1490

Funding

National Natural Science Foundation of China 82000126National Natural Science Foundation of China 82030005Postdoctoral Innovation Project of Shandong Province SDCX-ZG-202202023State Key Laboratory of Experimental Hematology Research Grant ZK23-02Taishan Scholar Foundation of Shandong Province ts20221157Taishan Scholar Foundation of Shandong Province tsqn202306350
6 · The paper itself

Abstract

backgroundVasculopathy is the most common complication of diabetes. Endothelial cells located in the innermost layer of blood vessels are constantly affected by blood flow or vascular components; thus, their mechanosensitivity plays an important role in mediating vascular regulation. Endothelial damage, one of the main causes of hyperglycemic vascular complications, has been extensively studied. However, the role of mechanosensitive signaling in hyperglycemic endothelial damage remains unclear.

methodsVascular endothelial-specific Piezo1 knockout mice were generated to investigate the effects of Piezo1 on Streptozotocin-induced hyperglycemia and vascular endothelial injury. In vitro activation or knockdown of Piezo1 was performed to evaluate the effects on the proliferation, migration, and tubular function of human umbilical vein endothelial cells in high glucose. Reactive oxygen species production, mitochondrial membrane potential alternations, and oxidative stress-related products were used to assess the extent of oxidative stress damage caused by Piezo1 activation.

resultsOur study found that in VE

conclusionIn summary, our study revealed that Piezo1 is involved in high glucose-induced oxidative stress injury and aggravated endothelial dysfunction, which have great significance for alleviating endothelial damage caused by hyperglycemia.

Indexed as

Blood GlucoseDiabetes Mellitus, ExperimentalHuman Umbilical Vein Endothelial CellsIon ChannelsMice, KnockoutNitric Oxide Synthase Type IIIOxidative StressAnimalsAorta, ThoracicApoptosisCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell MovementCell ProliferationCells, CulturedDiabetic AngiopathiesEndothelium, VascularBlood GlucoseCalcium-Calmodulin-Dependent Protein Kinase Type 2Ion ChannelsNFE2L2 protein, humanNfe2l2 protein, mouseNF-E2-Related Factor 2Nitric Oxide Synthase Type IIINos3 protein, mousePIEZO1 protein, humanPiezo1 protein, mouseReactive Oxygen SpeciesStreptozocinEndothelial dysfunctionHyperglycemiaNrf2Oxidative stressPiezo1

Identifiers

PMID38702777
PMCPMC11067304

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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.