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The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease

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...

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Autores principales: Wu, Ting, Zhou, Kaiyu, Hua, Yimin, Zhang, Wen, Li, Yifei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10157035/
https://www.ncbi.nlm.nih.gov/pubmed/37153765
http://dx.doi.org/10.3389/fphar.2023.1164487
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author Wu, Ting
Zhou, Kaiyu
Hua, Yimin
Zhang, Wen
Li, Yifei
author_facet Wu, Ting
Zhou, Kaiyu
Hua, Yimin
Zhang, Wen
Li, Yifei
author_sort Wu, Ting
collection PubMed
description 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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spelling pubmed-101570352023-05-05 The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease Wu, Ting Zhou, Kaiyu Hua, Yimin Zhang, Wen Li, Yifei Front Pharmacol Pharmacology 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. Frontiers Media S.A. 2023-04-20 /pmc/articles/PMC10157035/ /pubmed/37153765 http://dx.doi.org/10.3389/fphar.2023.1164487 Text en Copyright © 2023 Wu, Zhou, Hua, Zhang and Li. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Wu, Ting
Zhou, Kaiyu
Hua, Yimin
Zhang, Wen
Li, Yifei
The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease
title The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease
title_full The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease
title_fullStr The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease
title_full_unstemmed The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease
title_short The molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease
title_sort molecular mechanisms in prenatal drug exposure-induced fetal programmed adult cardiovascular disease
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10157035/
https://www.ncbi.nlm.nih.gov/pubmed/37153765
http://dx.doi.org/10.3389/fphar.2023.1164487
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