Evidence map›Paper›PMID 36611895›Full record

ArticleCells2022

Elabela: Negative Regulation of Ferroptosis in Trophoblasts via the Ferritinophagy Pathway Implicated in the Pathogenesis of Preeclampsia.

Huan Yang, Xuemei Zhang, Yubin Ding, Hui Xiong, Shaojian Xiang, Yang Wang, Huanhuan Li, Zheng Liu, Jie He, Yuelan Tao and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 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.

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  17. The Apelinergic System in Pregnancy.International journal of molecular sciences · 2023
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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 at 3 institutions in 1 country.

Huan YangDepartment of Obstetrics, Chongqing University Three Gorges Hospital, Chongqing 404100, China.ORCID 0000-0002-8308-4400
Xuemei ZhangJoint International Research Laboratory of Reproduction and Development of the Ministry of Education of China, Chongqing Medical University, Chongqing 400016, China.
Yubin DingJoint International Research Laboratory of Reproduction and Development of the Ministry of Education of China, Chongqing Medical University, Chongqing 400016, China.
Hui XiongDepartment of Obstetrics, Chongqing University Three Gorges Hospital, Chongqing 404100, China.
Shaojian XiangDepartment of Obstetrics, Chongqing University Three Gorges Hospital, Chongqing 404100, China.
Yang WangJoint International Research Laboratory of Reproduction and Development of the Ministry of Education of China, Chongqing Medical University, Chongqing 400016, China.
Huanhuan LiDepartment of Emergency, Chongqing University Three Gorges Hospital, Chongqing 404100, China.
Zheng LiuJoint International Research Laboratory of Reproduction and Development of the Ministry of Education of China, Chongqing Medical University, Chongqing 400016, China.
Jie HeJoint International Research Laboratory of Reproduction and Development of the Ministry of Education of China, Chongqing Medical University, Chongqing 400016, China.ORCID 0000-0002-2577-9247
Yuelan TaoJoint International Research Laboratory of Reproduction and Development of the Ministry of Education of China, Chongqing Medical University, Chongqing 400016, China.
Hongbing YangDepartment of Obstetrics, Chongqing University Three Gorges Hospital, Chongqing 404100, China.
Hongbo QiJoint International Research Laboratory of Reproduction and Development of the Ministry of Education of China, Chongqing Medical University, Chongqing 400016, China.
Chongqing University · CNThe Affiliated Yongchuan Hospital of Chongqing Medical University · CNChildren's Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preeclampsia is a leading contributor to increased maternal morbidity and mortality in the perinatal period. Increasing evidence demonstrates that ferroptosis is an essential mechanism for the pathogenesis of preeclampsia. Elabela is a novel small-molecule polypeptide, mainly expressed in embryonic and transplacental tissues, with an ability to promote cell proliferation and invasion. However, its specific regulatory mechanism in preeclampsia has not been completely elucidated. In this study, we first reveal an increased grade of ferroptosis accompanied by a downregulation of the expression of Elabela in preeclampsia placentas. We then confirm the presence of a ferroptosis phenotype in the placenta of the mouse PE-like model, and Elabela can reduce ferroptosis in the placenta and improve adverse pregnancy outcomes. Furthermore, we demonstrate that targeting Elabela alleviates the cellular dysfunction mediated by Erastin promoting increased lipid peroxidation in vitro. Subsequent mechanistic studies suggest that Elabela increases FTH1 levels by inhibiting the ferritinophagy pathway, and consequently chelates the intracellular labile iron pool and eventually arrests ferroptosis. In conclusion, Elabela deficiency exacerbates ferroptosis in the placenta, which is among the potential mechanisms in the pathogenesis of preeclampsia. Targeting the Elabela-ferritinophagy-ferroptosis signaling axis provides a new therapeutic intervention strategy to alleviate preeclampsia.

Indexed as

FerroptosisPre-EclampsiaAnimalsFemaleHumansMicePlacentaPregnancySignal TransductionTrophoblastsElabelaferritinophagyferroptosispreeclampsiatrophoblast

Identifiers

PMID36611895
PMCPMC9818811
OpenAlexW4312205653

What OpenQuestion holds

Textmetadata
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.