Evidence map›Paper›PMID 25575681›Full record

ArticleMolecular neurobiology2016

Developmental and Functional Brain Impairment in Offspring from Preeclampsia-Like Rats.

Xueyuan Liu, Wenlong Zhao, Haiyan Liu, Yaoyue Kang, Chen Ye, Weirong Gu, Rong Hu, Xiaotian Li

Open access · hybridAbstract read
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

41 citing papers in PubMed, 71 citations in OpenAlex.

  1. Exploring the Mechanism of Postpartum Cognitive Dysfunction in a Preeclampsia Rat Model via Multimodal Imaging.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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

8 authors at 4 institutions in 1 country.

Xueyuan LiuObstetrics and Gynecology Hospital of Fudan University, 200011, Shanghai, China.
Wenlong ZhaoUniversity of Chinese Academy of Sciences, Shanghai, 200031, China.
Haiyan LiuObstetrics and Gynecology Hospital of Fudan University, 200011, Shanghai, China.
Yaoyue KangDivision of Infectious Disease, Huashan Hospital, Fudan University, Shanghai, China.
Chen YeShanghai Changzheng Hospital, Second Military Medical University, Shanghai, China.
Weirong GuObstetrics and Gynecology Hospital of Fudan University, 200011, Shanghai, China. guweirong2013@163.com.
Rong HuObstetrics and Gynecology Hospital of Fudan University, 200011, Shanghai, China. hurongwy@sina.com.
Xiaotian LiObstetrics and Gynecology Hospital of Fudan University, 200011, Shanghai, China. xiaotianli2013@163.com.
Obstetrics and Gynecology Hospital of Fudan University · CNHuashan Hospital · CNShanghai Changzheng Hospital · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preeclampsia is associated with developmental delay in infants and with an increased risk of various diseases in adulthood, including hypertension and epilepsy. It has been reported that several organs show developmental retardation and functional deficiency in offspring of preeclamptic rats. However, the developmental and functional changes in brains of the offspring of preeclamptic rats remain unknown. Here, we established a preeclampsia-like rat model induced using Nω-nitro-L-arginine methyl ester (L-NAME) to analyze the developmental and functional changes in brains of the offspring. Body and brain weights were decreased in the L-NAME group at postnatal day 0 (P0). However, there were no significant differences between the L-NAME and control groups in brain and body weights at P56. Upon further analysis, we detected a deficiency in neurogenesis, but not in apoptosis, which contributed to the smaller brains of the offspring in the L-NAME group at P0. Additionally, we observed an increase in gliogenesis to compensate for the brain weights of the offspring at P56. Although the weight and laminar structure of the brains were essentially normal at P56, spatial learning and memory were severely impaired. We also found that adult hippocampal neurogenesis was disrupted in the offspring from preeclampsia-like rats, which may explain the cognitive deficiency. Moreover, qRT-PCR revealed a reduced expression of neurogenesis-related genes in the offspring. Overall, we have described the deleterious effects of preeclampsia on the brains of offspring, providing clues to the cellular and molecular mechanisms involved in this pathogenesis, which may aid in the development of therapeutic approaches.

Indexed as

AnimalsAnimals, NewbornApoptosisAstrocytesBrainCell ProliferationDisease Models, AnimalFemaleHippocampusLearningMemoryNeurogenesisNeurogliaNeuronsNG-Nitroarginine Methyl EsterPre-EclampsiaNG-Nitroarginine Methyl EsterAdult hippocampal neurogenesisGliogenesisL-NAMEPreeclampsia-likeWater maze

Identifiers

PMID25575681
PMCPMC4752589
OpenAlexW2074226823

What OpenQuestion holds

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Registered trials

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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.