Evidence map›Paper›PMID 31622511›Full record

ArticleBrain pathology (Zurich, Switzerland)2020

Complement C3a induces axonal hypomyelination in the periventricular white matter through activation of WNT/β-catenin signal pathway in septic neonatal rats experimentally induced by lipopolysaccharide.

Peixian Huang, Qiuping Zhou, Qiongyu Lin, Lanfen Lin, Huifang Wang, Xuan Chen, Shuqi Jiang, Hui Fu, Yiyu Deng

Open access · bronzeAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
11.7field-weighted citation impact, top 1% 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

23 citing papers in PubMed, 51 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Peixian HuangDepartment of Critical Care and Emergency, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, Guangdong, China.
Qiuping ZhouDepartment of Critical Care and Emergency, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, Guangdong, China.
Qiongyu LinDepartment of critical care medicine, Jieyang People's Hospital, Jieyang, 522000, Guangdong, China.
Lanfen LinDepartment of Critical Care and Emergency, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, Guangdong, China.
Huifang WangDepartment of Critical Care and Emergency, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, Guangdong, China.
Xuan ChenDepartment of Critical Care and Emergency, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, Guangdong, China.
Shuqi JiangDepartment of Critical Care and Emergency, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, Guangdong, China.
Hui FuDepartment of Anatomy, Wuhan University School of Basic Medical Sciences, Wuhan, 430072, Hubei, China.
Yiyu DengDepartment of Critical Care and Emergency, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, Guangdong, China.ORCID 0000-0002-0459-7399
Guangdong Academy of Medical Sciences · CNShantou University · CNWuhan University · CN

Funding

High-level Hospital Construction Project DFJH201804National Natural Science Foundation of China 81271329National Natural Science Foundation of China 81471237Natural Science Foundation of Guangdong Province 2019A1515010206
6 · The paper itself

Abstract

Neuroinflammation is thought to play a pivotal role in the pathogenesis of periventricular white matter (PWM) damage (PWMD) induced by neonatal sepsis. Because the complement cascade is implicated in inflammatory response, this study was carried out to determine whether C3a is involved in PWMD, and, if so, whether it would induce axonal hypomyelination. Furthermore, we explored if C3a would act through its C3a receptor (C3aR) and thence inhibit maturation of oligodendrocyte precursor cells (OPCs) via the WNT/β-catenin signal pathway. Sprague Dawley (SD) rats aged 1 day were intraperitoneally injected with lipopolysaccharide (LPS) (1 mg/kg). C3a was upregulated in activated microglia and astrocytes in the PWM up to 7 days after LPS injection. Concomitantly, enhanced C3aR expression was observed in NG2

Indexed as

AnimalsAnimals, NewbornCell DifferentiationCells, CulturedComplement C3aDemyelinating DiseasesLipopolysaccharidesMyelin SheathNeonatal SepsisOligodendrocyte Precursor CellsRatsRats, Sprague-DawleyUp-RegulationWhite MatterWnt Signaling PathwayComplement C3aLipopolysaccharidescomplement 3ahypomyelinationmicrogliasepsisWNT/β-catenin signaling

Identifiers

PMID31622511
PMCPMC8018074
OpenAlexW2981144016

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.