Evidence map›Paper›PMID 33082708›Full record

ReviewMediators of inflammation2020

The Role of Inflammation in the Pathogenesis of Preeclampsia.

Michał Michalczyk, Aleksander Celewicz, Marta Celewicz, Paula Woźniakowska-Gondek, Rafał Rzepka

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 7 pooled it
8.4field-weighted citation impact, top 2% 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

89 citing papers in PubMed, 7 syntheses or guidelines pooled it, 162 citations in OpenAlex.

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  14. Silibinin Modulates NF-κB Activation and Heat Shock Protein in Preeclampsia-Like Rat Model.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
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29 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Michał MichalczykDepartment of Gynecology and Obstetrics, Collegium Medicum, University of Zielona Góra, Zielona Góra, Poland.
Aleksander CelewiczDepartment of Gynecology and Obstetrics, Collegium Medicum, University of Zielona Góra, Zielona Góra, Poland.
Marta CelewiczDepartment of Obstetrics and Gynecology, Pomeranian Medical University, Szczecin, Poland.
Paula Woźniakowska-GondekDepartment of Gynecology and Obstetrics, Collegium Medicum, University of Zielona Góra, Zielona Góra, Poland.
Rafał RzepkaDepartment of Gynecology and Obstetrics, Collegium Medicum, University of Zielona Góra, Zielona Góra, Poland.ORCID https://orcid.org/0000-0002-9294-1005
University of Zielona Góra · PLPomeranian Medical University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preeclampsia (PE) affects 5-8% of pregnant women, and it is the major cause of perinatal morbidity and mortality. It is defined as arterial hypertension in women after 20 weeks of gestation which cooccurs with proteinuria (300 mg/d) or as arterial hypertension which is accompanied by one of the following: renal failure, liver dysfunction, hematological or neurological abnormalities, intrauterine growth restriction, or uteroplacental insufficiency. Currently, pathophysiology of preeclampsia poses a considerable challenge for perinatology. Preeclampsia is characterized by excessive and progressive activation of the immune system along with an increase in proinflammatory cytokines and antiangiogenic factors in fetoplacental unit as well as in vascular endothelium in pregnant women. A single, major underlying mechanism of preeclampsia is yet to be identified. This paper discusses the current understanding of the mechanisms which underlie the development of the condition. Some significant factors responsible for PE development include oxidative stress, abnormal concentration and activity in mononuclear phagocytic system, altered levels of angiogenic and antiangiogenic factors, and impaired inflammatory response triggered by inflammasomes. Detailed understanding of pathophysiology of inflammatory process in PE can largely contribute to new, targeted anti-inflammatory therapies that may improve perinatal outcomes in PE patients.

Indexed as

AnimalsFemaleHumansInflammationPlacentaPre-EclampsiaPregnancy

Identifiers

PMID33082708
PMCPMC7556088
OpenAlexW3090446993

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.