Cargando…
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...
Autores principales: | , , , , |
---|---|
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 |
_version_ | 1785036659669073920 |
---|---|
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. |
format | Online Article Text |
id | pubmed-10157035 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT wuting themolecularmechanismsinprenataldrugexposureinducedfetalprogrammedadultcardiovasculardisease AT zhoukaiyu themolecularmechanismsinprenataldrugexposureinducedfetalprogrammedadultcardiovasculardisease AT huayimin themolecularmechanismsinprenataldrugexposureinducedfetalprogrammedadultcardiovasculardisease AT zhangwen themolecularmechanismsinprenataldrugexposureinducedfetalprogrammedadultcardiovasculardisease AT liyifei themolecularmechanismsinprenataldrugexposureinducedfetalprogrammedadultcardiovasculardisease AT wuting molecularmechanismsinprenataldrugexposureinducedfetalprogrammedadultcardiovasculardisease AT zhoukaiyu molecularmechanismsinprenataldrugexposureinducedfetalprogrammedadultcardiovasculardisease AT huayimin molecularmechanismsinprenataldrugexposureinducedfetalprogrammedadultcardiovasculardisease AT zhangwen molecularmechanismsinprenataldrugexposureinducedfetalprogrammedadultcardiovasculardisease AT liyifei molecularmechanismsinprenataldrugexposureinducedfetalprogrammedadultcardiovasculardisease |