Evidence map›Paper›PMID 37292200›Full record

ArticleFrontiers in immunology2023

IL11 activates the placental inflammasome to drive preeclampsia.

Ellen Menkhorst, Leilani L Santos, Wei Zhou, Guannan Yang, Amy L Winship, Katarzyna E Rainczuk, Philana Nguyen, Jian-Guo Zhang, Paddy Moore, Michelle Williams and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.2field-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

13 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  4. Review
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  6. Review
  7. Late-Onset Preeclampsia is characterised by Accelerated Placental Aging.bioRxiv : the preprint server for biology · 2025
    Article
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  9. Review
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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

13 authors at 4 institutions in 1 country.

Ellen MenkhorstDepartment of Obstetrics and Gynaecology, The University of Melbourne, Parkville, VIC, Australia.
Leilani L SantosDepartment of Obstetrics and Gynaecology, The University of Melbourne, Parkville, VIC, Australia.
Wei ZhouDepartment of Obstetrics and Gynaecology, The University of Melbourne, Parkville, VIC, Australia.
Guannan YangDepartment of Obstetrics and Gynaecology, The University of Melbourne, Parkville, VIC, Australia.
Amy L WinshipCentre for Reproductive Health, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Katarzyna E RainczukCentre for Reproductive Health, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Philana NguyenDepartment of Obstetrics and Gynaecology, The University of Melbourne, Parkville, VIC, Australia.
Jian-Guo ZhangWalter and Eliza Hall Institute, Parkville, VIC, Australia.
Paddy MooreAbortion and Contraception, Royal Women's Hospital, Parkville, VIC, Australia.
Michelle WilliamsBiomedical Animal Facility, The University of Melbourne, Parkville, VIC, Australia.
Kim-Anh Lê CaoDepartment of Mathematics and Statistics, The University of Melbourne, Parkville, VIC, Australia.
Ashley MansellCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, VIC, Australia.
Evdokia DimitriadisDepartment of Obstetrics and Gynaecology, The University of Melbourne, Parkville, VIC, Australia.
The University of Melbourne · AUHudson Institute of Medical Research · AURoyal Women's Hospital · AUWalter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Preeclampsia is a life-threatening disorder of pregnancy unique to humans. Interleukin (IL)11 is elevated in serum from pregnancies that subsequently develop early-onset preeclampsia and pharmacological elevation of IL11 in pregnant mice causes the development of early-onset preeclampsia-like features (hypertension, proteinuria, and fetal growth restriction). However, the mechanism by which IL11 drives preeclampsia is unknown. Method: Pregnant mice were administered PEGylated (PEG)IL11 or control (PEG) from embryonic day (E)10-16 and the effect on inflammasome activation, systolic blood pressure (during gestation and at 50/90 days post-natal), placental development, and fetal/post-natal pup growth measured. RNAseq analysis was performed on E13 placenta. Human 1 Result: PEGIL11 activated the placental inflammasome causing inflammation, fibrosis, and acute and chronic hypertension in wild-type mice. Global and placental-specific loss of the inflammasome adaptor protein Asc and global loss of the Nlrp3 sensor protein prevented PEGIL11-induced fibrosis and hypertension in mice but did not prevent PEGIL11-induced fetal growth restriction or stillbirths. RNA-sequencing and histology identified that PEGIL11 inhibited trophoblast differentiation towards spongiotrophoblast and syncytiotrophoblast lineages in mice and extravillous trophoblast lineages in human placental villi. Discussion: Inhibition of ASC/NLRP3 inflammasome activity could prevent IL11-induced inflammation and fibrosis in various disease states including preeclampsia.

Indexed as

HypertensionPre-EclampsiaAnimalsFemaleFetal Growth RetardationFibrosisHumansInflammasomesInflammationInterleukin-11MiceNLR Family, Pyrin Domain-Containing 3 ProteinPlacentaPlacentationPregnancyInflammasomesInterleukin-11NLR Family, Pyrin Domain-Containing 3 ProteinASCfibrosishypertensioninflammasomeinterleukin 11NLRP3preeclampsia

Identifiers

PMID37292200
PMCPMC10244672
OpenAlexW4378072410

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.