ReviewFrontiers in pharmacology2023
The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease.
Review in Frontiers in pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Review
- A large-scale concordance study of toxicity findings across preclinical species and humans for small molecules and biologics.Frontiers in toxicology · 2026Article
- Development and Validation of a Predictive Screening Model for Congenital Heart Disease in High-Altitude Children.Risk management and healthcare policy · 2026Article
- A Disintegrin and Metalloprotease with Thrombospondin Motif, Member 13, and Von Willebrand Factor in Relation to the Duality of Preeclampsia and HIV Infection.International journal of molecular sciences · 2025Review
- Programming the heart: prenatal glucocorticoids and sex-specific cardiovascular risk.American journal of physiology. Heart and circulatory physiology · 2025Article
- Article
- Research trends in lipid-lowering therapies for coronary heart disease combined with hyperlipidemia: a bibliometric study and visual analysis.Frontiers in pharmacology · 2024Article
- The predictive value of the triglyceride glucose index combined with cystatin C for the prognosis of patients with acute coronary syndrome.Frontiers in endocrinology · 2024Article
- The Epigenetic Legacy of Maternal Protein Restriction: RenalNutrients · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The "developmental origins of health and disease" (DOHaD) hypothesis posits that early-life environmental exposures have a lasting impact on individual's health and permanently shape growth, structure, and metabolism. This reprogramming, which results from fetal stress, is believed to contribute to the development of adulthood cardiovascular diseases such as hypertension, coronary artery disease, heart failure, and increased susceptibility to ischemic injuries. Recent studies have shown that prenatal exposure to drugs, such as glucocorticoids, antibiotics, antidepressants, antiepileptics, and other toxins, increases the risk of adult-onset cardiovascular diseases. In addition, observational and animal experimental studies have demonstrated the association between prenatal drug exposure and the programming of cardiovascular disease in the offspring. The molecular mechanisms underlying these effects are still being explored but are thought to involve metabolism dysregulation. This review summarizes the current evidence on the relationship between prenatal drug exposure and the risk of adult cardiovascular disorders. Additionally, we present the latest insights into the molecular mechanisms that lead to programmed cardiovascular phenotypes after prenatal drug exposure.
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Registered trials
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.