Evidence map›Paper›PMID 38731818›Full record

ReviewInternational journal of molecular sciences2024

The Impact of the Aryl Hydrocarbon Receptor on Antenatal Chemical Exposure-Induced Cardiovascular-Kidney-Metabolic Programming.

You-Lin Tain, Chien-Ning Hsu

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Epigenetic Consequences of In Utero PFAS Exposure: Implications for Development and Long-Term Health.International journal of environmental research and public health · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Review
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

2 authors.

You-Lin TainDivision of Pediatric Nephrology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.ORCID 0000-0002-7059-6407
Chien-Ning HsuDepartment of Pharmacy, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.ORCID 0000-0001-7470-528X

Funding

Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan CMRPG8M0752, CMRPG8M0721, CMRPG8M0722, CORPG8P0031, CMRPG8P0081, and CORPG8P0011
6 · The paper itself

Abstract

Early life exposure lays the groundwork for the risk of developing cardiovascular-kidney-metabolic (CKM) syndrome in adulthood. Various environmental chemicals to which pregnant mothers are commonly exposed can disrupt fetal programming, leading to a wide range of CKM phenotypes. The aryl hydrocarbon receptor (AHR) has a key role as a ligand-activated transcription factor in sensing these environmental chemicals. Activating AHR through exposure to environmental chemicals has been documented for its adverse impacts on cardiovascular diseases, hypertension, diabetes, obesity, kidney disease, and non-alcoholic fatty liver disease, as evidenced by both epidemiological and animal studies. In this review, we compile current human evidence and findings from animal models that support the connection between antenatal chemical exposures and CKM programming, focusing particularly on AHR signaling. Additionally, we explore potential AHR modulators aimed at preventing CKM syndrome. As the pioneering review to present evidence advocating for the avoidance of toxic chemical exposure during pregnancy and deepening our understanding of AHR signaling, this has the potential to mitigate the global burden of CKM syndrome in the future.

Indexed as

Cardiovascular DiseasesPrenatal Exposure Delayed EffectsReceptors, Aryl HydrocarbonAnimalsEnvironmental PollutantsFemaleFetal DevelopmentHumansKidneyKidney DiseasesMaternal ExposureMetabolic ReprogrammingPregnancySignal TransductionEnvironmental PollutantsReceptors, Aryl Hydrocarbonaryl hydrocarbon receptorcardiovascular diseasechemicalchronic kidney diseasedevelopmental origins of health and disease (DOHaD)dioxinshypertensionmetabolic syndromeprenatal exposure

Identifiers

PMID38731818
PMCPMC11083012

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.