Evidence map›Paper›PMID 38569482›Full record

ArticleGynecologic and obstetric investigation2024

Exogenous Hydrogen Sulfide Prevents Necroptosis by Inhibiting p38MAPK Pathway Activation in JEG-3 Trophoblast Cells: A Role in Preeclampsia.

Caihong Zhang, Zixi Chen, Huijing Shao, Ziwen Ma, Rui Guan, Xiaomin Yu, Qianqian Sun, Hang Gu

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

Article in Gynecologic and obstetric investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. Recent advances in the role of gasotransmitters in necroptosis.Apoptosis : an international journal on programmed cell death · 2025
    Review
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.

Caihong ZhangDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Zixi ChenDepartment of Laboratory Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Huijing ShaoDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Ziwen MaDepartment of Obstetrics and Gynecology, New Area Health Care Hospital Fore Women and Children, Shanghai, China.
Rui GuanDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Xiaomin YuDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Qianqian SunDepartment of Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, China.
Hang GuDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Shanghai First Maternity and Infant Hospital · CNShanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesNecroptosis, a form of programmed cell death, can occur in the placenta of patients with preeclampsia (PE). Hydrogen sulfide (H2S) can inhibit necroptosis of human umbilical vein endothelial cells under the high glucose-induced injury. Whether H2S can protect trophoblasts against necroptosis underlying PE has not been elucidated. This study aimed to explore the protective role of H2S in trophoblast cells against necroptosis underlying PE.

designThis is an in vitro experimental study.

participantsA total of 10 pregnant women with severe PE and 10 matched control normotensive pregnant women were included. The placenta tissues were extracted from participators. The human JEG-3 trophoblasts were commercially available.

methodsThe expression and localization of necrotic proteins were assayed in human placenta samples, and the effect of necrotic cell death on the proliferation and apoptosis of human JEG-3 trophoblasts was evaluated. The component expressions of inflammatory cytokine and p38MAPK signaling pathway were measured in samples pretreated with or without NaHS (H2S donor) and SB203580 (p38 inhibitor).

resultsRIPA1, RIPA3, and p-p38 levels were significantly higher in PE placental tissue, whereas cystathionine β-synthase expression was decreased. In JEG-3 trophoblasts, necroptosis increased apoptotic cell numbers, suppressed cell proliferation, increased inflammatory cytokine expression, and increased p38MAPK activation, which can be prevented by NaHS. LIMITATIONS: In the present study, we did not provide sufficient evidence that necroptosis was a part of the pathogenesis of PE.

conclusionsWe proposed the putative role of necroptosis in early-onset PE, reflected by the blockage of caspase-8/3 and increased expression of RIPA1 and RIPA3 in PE placenta tissues. Furthermore, we demonstrated that exogenous H2S protected cytotrophoblasts against ceramide-induced necroptosis via the p38MAPK pathway.

Indexed as

Hydrogen SulfideNecroptosisp38 Mitogen-Activated Protein KinasesPre-EclampsiaTrophoblastsAdultApoptosisCase-Control StudiesCell LineFemaleHumansImidazolesMAP Kinase Signaling SystemPlacentaPregnancyHydrogen SulfideImidazolesp38 Mitogen-Activated Protein KinasesCytotrophoblastHydrogen sulfideNecroptosisp38MAPKPreeclampsia

Identifiers

PMID38569482
PMCPMC11446324
OpenAlexW4394741113

What OpenQuestion holds

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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.