Evidence map›Paper›PMID 30543046›Full record

ArticleInflammation2019

Intrauterine Inflammation Damages Placental Angiogenesis via Wnt5a-Flt1 Activation.

F Xu, Z X Ren, X M Zhong, Q Zhang, J Y Zhang, J Yang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  3. Bioinformatics analysis explores key pathways and hub genes in central precocious puberty.Journal of pediatric endocrinology & metabolism : JPEM · 2025
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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

6 authors at 1 institution in 1 country.

F XuDepartment of Neonatology, Guangdong Women and Children Hospital, Guang Zhou Medical University, Guangzhou, 510010, Guangdong, China.
Z X RenDepartment of Neonatology, Guangdong Women and Children Hospital, Guang Zhou Medical University, Guangzhou, 510010, Guangdong, China.
X M ZhongDepartment of Neonatology, Guangdong Women and Children Hospital, Guang Zhou Medical University, Guangzhou, 510010, Guangdong, China.
Q ZhangDepartment of Clinical Genetic Center, Guangdong Women and Children Hospital, Guangzhou, 510010, Guangdong, China.
J Y ZhangDepartment of Pathology, Guangdong Women and Children Hospital, Guang Zhou Medical University, Guangzhou, 510010, Guangdong, China.
J YangDepartment of Neonatology, Guangdong Women and Children Hospital, Guang Zhou Medical University, Guangzhou, 510010, Guangdong, China. jieyang0830@163.com.ORCID http://orcid.org/0000-0002-7051-0597
Guangdong Province Women and Children Hospital · CN

Funding

Guangzhou Science and Technology Program key projects 201707010398Guangzhou Science, Technology and Innovation Commission 201804010380National Natural Science Foundation of China 81873847
6 · The paper itself

Abstract

Intrauterine inflammation is the main reason for neonatal adverse outcomes and normal placenta perfusion plays an important role in fetal development. However, whether inflammation will affect placental angiogenesis and the underlying mechanism are still poorly understood. To investigate lipopolysaccharide (LPS)-induced intrauterine inflammation on placenta angiogenesis and Wnt5a-Flt1 expression. LPS-induced intrauterine inflammation rat model was established. Preterm rat outcomes were analyzed and angiogenesis of placenta villi was calculated by immunohistochemistry (IHC) of CD34 staining, and placenta Wnt5a-Flt1 expression was detected by western blot and IHC. Compared to control group, neonatal rats in LPS group showed higher death rate (1.4% vs 10.1%, p < 0.05) and lower birth weight (6.36 ± 0.48 vs 5.70 ± 0.67, p < 0.01); the villi vessel area and mean diameter in the placenta were significantly reduced in the LPS group (total area %, 16.7% ± 0.6% vs 8.7% ± 0.4%, p < 0.01, n = 9; mean diameter (pixel), 15.6 ± 0.5 vs 12.9 ± 0.3, p < 0.01, n = 9). Placenta Wnt5a-Flt1 expression was upregulated significantly (integrated optical density (IOD) in IHC: Wnt5a, 1667 ± 1204 vs 11,076 ± 4046, p < 0.05; Flt1, 2554 ± 466.2 vs 7998 ± 1613, p < 0.05; western blot: Wnt5a, 0.33 ± 0.05 vs 0.96 ± 0.06, p < 0.05; Flt1, 0.36 ± 0.15 vs 1.08 ± 0.08, p < 0.05). Intrauterine inflammation gave rise to offspring death rate and low birth weight; the mechanism might be disordered placental angiogenesis via Wnt5a-Flt1 activation triggered by inflammation.

Indexed as

AnimalsAnimals, NewbornBirth WeightFemaleInflammationLipopolysaccharidesMortalityNeovascularization, PathologicPlacentaPregnancyRatsUp-RegulationUterusVascular Endothelial Growth Factor Receptor-1Wnt-5a ProteinFlt1 protein, ratLipopolysaccharidesVascular Endothelial Growth Factor Receptor-1Wnt-5a ProteinWnt5a protein, ratangiogenesisFlt1intrauterine inflammationplacentapretermWnt5a

Identifiers

PMID30543046
OpenAlexW2905038176

What OpenQuestion holds

Textmetadata
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.