Evidence map›Paper›PMID 35091806›Full record

ArticleCell and tissue research2022

Esomeprazole inhibits hypoxia/endothelial dysfunction-induced autophagy in preeclampsia.

Shengyi Gu, Chenchen Zhou, Jindan Pei, Yuelin Wu, Sheng Wan, Xiaobo Zhao, Junhao Hu, Xiaolin Hua

Open access · hybridAbstract read
In one paragraph

Article in Cell and tissue research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  9. Article
  10. Secondary prevention of preeclampsia.Frontiers in cell and developmental biology · 2025
    Review
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  12. Article
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  18. NLRP3 inhibition improves maternal hypertension, inflammation, and vascular dysfunction in response to placental ischemia.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Article
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 2 institutions in 1 country.

Shengyi Gu *Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Chenchen Zhou *Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Jindan Pei *Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Yuelin WuShanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Sheng WanShanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Xiaobo ZhaoShanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Junhao HuInterdisciplinary Research Center On Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, 201203, China.
Xiaolin HuaShanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China. xiaolin_hua@tongji.edu.cn.ORCID http://orcid.org/0000-0003-1098-5010
Shanghai First Maternity and Infant Hospital · CNChinese Academy of Sciences · CN

Funding

Health and Family Planning Committee of Pudong New Area PW2019D-13National Natural Science Foundation of China 81873816National Natural Science Foundation of China 82071629Shanghai Development Center SHDC2020CR6021Shanghai Municipal Health Commission 202040128
6 · The paper itself

Abstract

Preeclampsia (PE) affects 3 to 5% of pregnant women worldwide and is associated with fetal and maternal morbidity and mortality. Although a complete understanding of PE remains elusive, it has been widely accepted that a dysfunction of the placenta plays a key role in the pathogenesis of PE. In this study, we investigated the role of excessive placental autophagy during PE pathogenesis and explored whether esomeprazole ameliorates PE by inhibiting the autophagy in the placenta. The PE cellular model was established by treating the cells' L-NAME and hypoxia. The PE mice model was established by L-NAME administration and was confirmed by the increased systolic blood pressure (SBP) and urinary protein detected. The autophagy and key proteins were detected in human placental tissue, in cells, and in the mice model by Western blot and immunofluorescence staining. Results showed that excessive autophagy could be detected in human PE placental tissue, in the PE cellular model, and in the PE mice model. Hypoxia induces autophagy by activating AMPKα and inhibiting mTOR in vivo and in vitro. Esomeprazole inhibits L-NAME-induced autophagy in mice by inhibiting AMPKα and activating mTOR. In conclusion, this study demonstrates that the excessive autophagy induced by the SIRT1/AMPKα-mTOR pathway plays a significant role in the pathogenesis of PE. However, esomeprazole treatment inhibits AMPKα but activates mTOR, resulting in the inhibition of autophagy in the placenta and, therefore, mitigates PE symptoms.

Indexed as

EsomeprazolePre-EclampsiaAnimalsAutophagyFemaleHumansHypoxiaMicePlacentaPregnancyEsomeprazoleAMPKα-mTORAutophagyEsomeprazolePlacentaPreeclampsia

Identifiers

PMID35091806
PMCPMC8976802
OpenAlexW4210257858

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.