Evidence map›Paper›PMID 39351527›Full record

ReviewFrontiers in endocrinology2024

Prenatal glucocorticoids exposure and adverse cardiovascular effects in offspring.

Chenxuan Zhao, Lei He, Lingjun Li, Fengying Deng, Meihua Zhang, Changhong Wang, Junlan Qiu, Qinqin Gao

Abstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. [Development of an LC-MS/MS method for 32 steroid hormones and exploration of their gestational variations].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  8. Article
  9. Review
  10. Review
  11. Programming the heart: prenatal glucocorticoids and sex-specific cardiovascular risk.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  12. Review
  13. Article
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.

Chenxuan Zhao *Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
Lei He *Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
Lingjun Li *Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
Fengying DengInstitute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
Meihua ZhangKey Laboratory of Birth Regulation and Control Technology of National Health Commission of China, Shandong Provincial Maternal and Child Health Care Hospital Affiliated to Qingdao University, Jinan, China.
Changhong WangGenetics and Prenatal Diagnosis Center, Fuyang People's Hospital, Fuyang, China.
Junlan QiuDepartment of Oncology and Hematology, Suzhou Hospital, Affiliated Hospital of Medical School, Nanjing University, Suzhou, Jiangsu, China.
Qinqin GaoInstitute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoids (GCs) are steroid hormones fundamental to the body's normal physiological functions and are pivotal in fetal growth and development. During gestation, the mother's cortisol concentration (active GCs) escalates to accommodate the requirements of fetal organ development and maturation. A natural placental GCs barrier, primarily facilitated by 11β hydroxysteroid dehydrogenase 2, exists between the mother and fetus. This enzyme transforms biologically active cortisol into biologically inactive corticosterone, thereby mitigating fetal GCs exposure. However, during pregnancy, the mother may be vulnerable to adverse factor exposures such as stress, hypoxia, caffeine, and synthetic GCs use. In these instances, maternal serum GCs levels may surge beyond the protective capacity of the placental GCs barrier. Moreover, these adverse factors could directly compromise the placental GCs barrier, resulting in excessive fetal exposure to GCs. It is well-documented that prenatal GCs exposure can detrimentally impact the offspring's cardiovascular system, particularly in relation to blood pressure, vascular function, and heart function. In this review, we succinctly delineate the alterations in GCs levels during pregnancy and the potential mechanisms driving these changes, and also analyze the possible causes of prenatal GCs exposure. Furthermore, we summarize the current advancements in understanding the adverse effects and mechanisms of prenatal GCs exposure on the offspring's cardiovascular system.

Indexed as

GlucocorticoidsPrenatal Exposure Delayed EffectsAnimalsCardiovascular DiseasesCardiovascular SystemFemaleFetal DevelopmentHumansPlacentaPregnancyGlucocorticoids11β hydroxysteroid dehydrogenase 2cardiovascular systemoffspringplacental GCs barrierprenatal GCs exposure

Identifiers

PMID39351527
PMCPMC11439645

What Socratic 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 Socratic graph.