Evidence map›Paper›PMID 37891193›Full record

ArticleScientific reports2023

Preliminary evidence that blocking the uptake of placenta-derived preeclamptic extracellular vesicles protects the vascular endothelium and prevents vasoconstriction.

Lena Erlandsson, Lena Ohlsson, Zahra Masoumi, Mimmi Rehnström, Tina Cronqvist, Lars Edvinsson, Stefan R Hansson

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 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
5.0field-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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Extracellular vesicles in preeclampsia: drivers of vascular dysfunction and inflammation.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  8. Article
  9. EngineeredInternational journal of nanomedicine · 2025
    Article
  10. Proteomic Profiles of Maternal Plasma Extracellular Vesicles for Prediction of Preeclampsia.American journal of reproductive immunology (New York, N.Y. : 1989) · 2024
    Article
  11. Article
  12. Review
  13. 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

7 authors at 2 institutions in 1 country.

Lena Erlandsson *Division of Obstetrics and Gynecology, Department of Clinical Sciences Lund, Lund University, BMC C14, Klinikgatan 28, 221 85, Lund, Sweden. lena.erlandsson@med.lu.se.
Lena Ohlsson *Experimental Vascular Research, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
Zahra MasoumiDivision of Obstetrics and Gynecology, Department of Clinical Sciences Lund, Lund University, BMC C14, Klinikgatan 28, 221 85, Lund, Sweden.
Mimmi RehnströmDivision of Obstetrics and Gynecology, Department of Clinical Sciences Lund, Lund University, BMC C14, Klinikgatan 28, 221 85, Lund, Sweden.
Tina CronqvistDivision of Obstetrics and Gynecology, Department of Clinical Sciences Lund, Lund University, BMC C14, Klinikgatan 28, 221 85, Lund, Sweden.
Lars EdvinssonExperimental Vascular Research, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
Stefan R HanssonDivision of Obstetrics and Gynecology, Department of Clinical Sciences Lund, Lund University, BMC C14, Klinikgatan 28, 221 85, Lund, Sweden.
Lund University · SESkåne University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preeclampsia (PE) is a pregnancy syndrome characterized by hypertension and organ damage manifesting after 20 gestational weeks. The etiology is of multifactorial origin, where placental stress causes increased levels of placenta-derived extracellular vesicles (STBEVs) in the maternal circulation, shown to cause inflammation, endothelial activation, vasoconstriction, and anti-angiogenic activity. General endothelial dysfunction is believed to be initiated by endothelial insult during pregnancy that alters vascular function resulting in increased arterial stiffness, cardiac dysfunction, and increased risk of cardiovascular disease later in life. We compared the effect of normal and PE derived STBEVs in vitro on vascular contractility of human subcutaneous arteries using wire myography. Cellular structures of exposed vessels were investigated by transmission electron microscopy. We explored strategies to pharmacologically block the effects of the STBEVs on human vessels. The PE STBEVs caused significantly stronger angiotensin II-mediated contractions and extended structural damage to human subcutaneous arteries compared to normal STBEVs. These negative effects could be reduced by blocking vesicle uptake by endothelial cells, using chlorpromazine or specific antibodies towards the LOX-1 receptor. The therapeutic potential of blocking vesicle uptake should be further explored, to reduce the permanent damage caused on the vasculature during PE pregnancy to prevent future cardiovascular risk.

Indexed as

Extracellular VesiclesPre-EclampsiaEndothelial CellsEndothelium, VascularFemaleHumansPlacentaPregnancyVasoconstriction

Identifiers

PMID37891193
PMCPMC10611745
OpenAlexW4387996943

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.