Evidence map›Paper›PMID 29493455›Full record

ReviewCurrent vascular pharmacology2019

Effects of Estrogen in Gender-dependent Fetal Programming of Adult Cardiovascular Dysfunction.

Zewen Chen, Lei Wang, Jun Ke, Daliao Xiao

Abstract readReview
In one paragraph

Review in Current vascular pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-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

10 citing papers in PubMed, 9 citations in OpenAlex.

  1. Carrageenan-induced immunothrombotic models in rodents (Review).Experimental and therapeutic medicine · 2026
    Review
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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

4 authors at 1 institution in 1 country.

Zewen ChenCenter for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, United States.
Lei WangCenter for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, United States.
Jun KeCenter for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, United States.
Daliao XiaoCenter for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, United States.
Loma Linda University · US

Funding

Maternal inhaled nicotine leads to aberrant development of hypertensive phenotypeR01HL135623 · NHLBI · LOMA LINDA UNIVERSITY · PI SHAO, XUESI MAX, XIAO, DALIAO · 2017 to 2021
$2.3M
miRNA as a novel therapeutic target in antenatal nicotine-induced ischemic heartR01HD088039 · NICHD · LOMA LINDA UNIVERSITY · PI XIAO, DALIAO · 2017 to 2021
$1.6M
Nicotine-mediated fetal programming of vascular dysfunction phenotypeR03DA041492 · NIDA · LOMA LINDA UNIVERSITY · PI XIAO, DALIAO · 2017 to 2018
$158k
NHLBI NIH HHS R01 HL135623NICHD NIH HHS R01 HD088039NIDA NIH HHS R03 DA041492
6 · The paper itself

Abstract

backgroundEpidemiological studies and experimental studies have demonstrated that intrauterine adverse environment increases the risk of Cardiovascular Disease (CVD) in adulthood. However, whether an individual develops a cardiovascular dysfunctional phenotype may depend on genetic background, age, and sex.

methodsIn this review, we summarize some of the recent experimental animal studies in the developmental programming of adult CVD with an emphasis on sex differences and the potential role of estrogen in mediating sexual dimorphism.

resultsFew epidemiological studies report the effect of sex on the developmental programming of CVD. However, numerous experimental animal studies have shown a sex difference in fetal programming of adult cardiovascular dysfunction. Most of the animal studies indicate that male offspring develop cardiovascular dysfunction and CVD in adulthood, whereas adult females appear to be protected. Estrogen is one of the key factors that contributes to the sex difference of adult CVD. Estrogen/its Receptor (ER) may interact with the RAS system by changes of DNA methylation patterns at the target gene promoter, serve as an antioxidant to counteract the prenatal insults-induced heightened ROS, and function as an eNOS activator to increase vasodilation, resulting in the protection of female offspring from the development of hypertension and other CVDs.

conclusionThese studies suggest that estrogen/ER may contribute to sex differences in cardiovascular response to an adverse intrauterine environment and play a significant role in modulating the cardiovascular response in adulthood.

Indexed as

Prenatal Exposure Delayed EffectsAge FactorsAnimalsCardiovascular DiseasesCardiovascular SystemEstrogensFemaleFetal DevelopmentGene Expression Regulation, DevelopmentalHemodynamicsHumansMalePregnancyRisk AssessmentRisk FactorsSex CharacteristicsEstrogensblood pressurecardiovascular dysfunctionestrogenfetal programminghypertensive.Sex difference

Identifiers

PMID29493455
PMCPMC6193848
OpenAlexW2794285324

What OpenQuestion holds

Textmetadata
LicenceTDM
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.