Evidence map›Paper›PMID 40986011›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2025

taVNS alleviates preeclampsia-induced vascular endothelial dysfunction via α7nAChR- IP3R1/GRP75/VDAC1 signal pathway.

Jing Zhao, Yuman Lei, Chengcheng Mu, Yuwei Wu, Rourou Fang, Dongdong Wu, Shouzhu Xu, Haifa Qiao

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. 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

8 authors.

Jing ZhaoInstitute for Chinese Medicine Frontier Interdisciplinary Science and Technology, Shaanxi University of Chinese Medicine, Xixian New Area, 712046, China.
Yuman LeiDepartment of Public Health, Shaanxi University of Chinese Medicine, Xixian New Area, 712046, China.
Chengcheng MuCollege of Medical Technology, Shaanxi University of Chinese Medicine, Xixian New Area, 712046, China.
Yuwei WuInstitute for Chinese Medicine Frontier Interdisciplinary Science and Technology, Shaanxi University of Chinese Medicine, Xixian New Area, 712046, China.
Rourou FangDepartment of Public Health, Shaanxi University of Chinese Medicine, Xixian New Area, 712046, China.
Dongdong WuDepartment of Public Health, Shaanxi University of Chinese Medicine, Xixian New Area, 712046, China.
Shouzhu XuDepartment of Public Health, Shaanxi University of Chinese Medicine, Xixian New Area, 712046, China. xsz90026@163.com.
Haifa QiaoInstitute for Chinese Medicine Frontier Interdisciplinary Science and Technology, Shaanxi University of Chinese Medicine, Xixian New Area, 712046, China. 1511006@sntcm.edu.cn.

Funding

Innovation Capability Support Program of Xianyang Program No. L2024-CXNL-KJRCTD-KJRC-0015Key Research and Development Program Project of Shaanxi Province grant no. 2024SF-YBXM-471National Natural Science Foundation of China 82105016, 82100488, 82205263Scientific Research Fund Project of Shaanxi Province Department of Education 21JS012
6 · The paper itself

Abstract

backgroundEndothelial dysfunction is considered to play a pivotal role in the pathogenesis of preeclampsia (PE). Transcutaneous auricular vagus nerve stimulation (taVNS) is a potential non-pharmaceutical alternative treatment for PE. This study aimed to explore the mechanisms of taVNS on endothelial dysfunction.

methodsWe used the reduced uterine perfusion pressure method to establish PE model and TNF-α to establish endothelial dysfunction model in HUVECs. In vivo, we detected blood pressure, vascular proteomics and morphology, ACh and receptor α7nAChR, and inflammatory factors (IL-6, IL-1β, and TNF-α). In vitro, we checked cell viability, mitochondrial membrane potential, apoptosis rate, calcium levels, HUVECs morphology, and Endoplasmic reticulum (ER) and mitochondria (MITO) interaction.

resultstaVNS promoted the release of ACh, which decreased Ca

conclusiontaVNS may exert an anti-PE effect through ER-MITO interaction. These findings offer preliminary insights into PE pathogenesis, and suggest that the ACh/α7nAChR axis and IP3R1/GRP75/VDAC1 complex could be promising targets for future therapeutic investigation.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorEndothelium, VascularPre-EclampsiaAnimalsApoptosisCalciumFemaleHumansHuman Umbilical Vein Endothelial CellsInositol 1,4,5-Trisphosphate ReceptorsMembrane ProteinsMitochondriaPregnancySignal TransductionVoltage-Dependent Anion Channel 1alpha7 Nicotinic Acetylcholine ReceptorCalciumInositol 1,4,5-Trisphosphate ReceptorsMembrane ProteinsVDAC1 protein, humanVoltage-Dependent Anion Channel 1Alpha 7 nicotinic acetylcholine receptorIP3R1/GRP75/VDAC1 complexPreeclampsiaTranscutaneous auricular vagus nerve stimulationVascular endothelial dysfunction

Identifiers

PMID40986011

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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.