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Mechanisms and Effects of Endocrine Disruptors and Environmental Contaminants on Cardiovascular Health

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 260

Special Issue Editor


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Guest Editor
RISE-Health, Department of Medical Sciences, Faculty of Health Sciences, University of Beira Interior, 6200-506 Covilha, Portugal
Interests: endocrine-disrupting chemicals; pregnant women; vascular homeostasis; human umbilical artery; smooth muscle cells; octylmethoxycinnamate
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Special Issue Information

Dear Colleagues,

Human exposure to emerging contaminants with the action of endocrine-disrupting compounds (EDCs) is a major of concern. Despite efforts by the scientific community, their toxic effects on human cardiovascular health remain largely unknown. Their modes of action involve EATS modalities (estrogenic, androgenic, steroidogenic, and thyroid) as well as non-EATS modalities, capable of triggering adverse outcomes (AOs). Clarifying the mechanisms by which EDCs affect cardiovascular health is crucial for effective risk assessment. The adverse outcome pathway (AOP) framework helps identify key events leading to AOs, while New Approach Methodologies (NAMs) provide innovative tools for this assessment. According to the one health approach, the interconnectedness of human, animal and environmental health highlights the need for integrated strategies to mitigate the impact of these emerging contaminants. In this sense, in this Special Issue, we invite you to provide updated insights on this topic. Reviews and research articles that aim to clarify the molecular and cellular mechanisms underlying the cardiovascular toxicity effects induced by EDCs are welcome.

Dr. Margarida Lorigo
Guest Editor

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Keywords

  • environmental exposure
  • emerging compounds
  • human health
  • risk assessment
  • adverse outcome pathway
  • new approach methodologies
  • one health

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Published Papers (1 paper)

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Research

18 pages, 1818 KiB  
Article
Bisphenol A Exposure Modifies the Vasoactive Response of the Middle Cerebral Artery
by Henrique Eloi Costa, Margarida Lorigo and Elisa Cairrao
Int. J. Mol. Sci. 2025, 26(8), 3896; https://doi.org/10.3390/ijms26083896 - 20 Apr 2025
Viewed by 161
Abstract
Bisphenol A (BPA) is the most used widely synthetic compound for the manufacture of polycarbonate plastics and epoxy resins produced worldwide. Given its androgenic and estrogenic activities, BPA is an endocrine disruptor that is linked to neurological and vascular outcomes, including strokes. Therefore, [...] Read more.
Bisphenol A (BPA) is the most used widely synthetic compound for the manufacture of polycarbonate plastics and epoxy resins produced worldwide. Given its androgenic and estrogenic activities, BPA is an endocrine disruptor that is linked to neurological and vascular outcomes, including strokes. Therefore, this study aims to investigate the mechanisms by which a 24 h exposure to BPA (0.002–20 μM) modifies the contractile function of rat middle cerebral artery (MCA) smooth muscle cells (SMCs). Thus, MCA explants were isolated from Wistar rats, and the SMC-MCA vasoactive response was assessed using planar cell surface area, while the gene expression of proteins and ion channel subunits involved in the MCA vasoactive response was evaluated by real-time quantitative PCR. The exposure to BPA (0.02 and 2 μM) decreased the noradrenaline (NA) vasocontractile response and sodium nitroprusside (SNP) vasorelaxant response. Moreover, exposure to BPA (0.02 and 2 μM) increased the gene expression of the soluble guanyl cyclase protein and the large conductance Ca2+-activated K+ channels (1.1 α-subunit). These results suggest an impairment of the SMC-MCA vasoactive response induced by intermediate BPA concentrations, an effect not attained for the lowest or highest exposure concentrations (non-monotonic inverted U-shaped response). In summary, these findings suggest that BPA exposure modifies MCA vascular homeostasis by interfering with the nitric oxide (NO) pathway and may, thus, be involved in ischemic stroke development. Full article
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