ArticleBiomolecules2021
Bisphenol A Induces Accelerated Cell Aging in Murine Endothelium.
Article in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 35 citations in OpenAlex.
- Environmental endocrine disruptors in cardio-oncology: emerging modifiers of cardiovascular vulnerability in patients with cancer.Cardio-oncology (London, England) · 2026Review
- Article
- Exploring the pathophysiological relationship between bisphenol A exposure and ischemic stroke risk using network toxicology and machine learning.BMC neurology · 2025Article
- Bisphenol-A disrupts mitochondrial functionality leading to senescence and apoptosis in human amniotic mesenchymal stromal cells.Cell death discovery · 2025Article
- The commonly used antibiotic streptomycin reduces protein synthesis and differentiation in cultured C2C12 myotubes.Physiological reports · 2025Article
- Article
- Combination of Bisphenol A and Its Emergent Substitute Molecules Is Related to Heart Disease and Exerts a Differential Effect on Vascular Endothelium.International journal of molecular sciences · 2023Article
- Screening of Metabolism-Disrupting Chemicals on Pancreatic α-Cells Using In Vitro Methods.International journal of molecular sciences · 2022Article
- Association between urinary concentrations of bisphenol A substitutes and diabetes in adults.World journal of diabetes · 2022Article
- Endocrine-Disrupting Chemicals and Their Adverse Effects on the Endoplasmic Reticulum.International journal of molecular sciences · 2022Review
- Identification and validation of senescence-related genes in circulating endothelial cells of patients with acute myocardial infarction.Frontiers in cardiovascular medicine · 2022Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bisphenol A (BPA) is a widespread endocrine disruptor affecting many organs and systems. Previous work in our laboratory demonstrated that BPA could induce death due to necroptosis in murine aortic endothelial cells (MAECs). This work aims to evaluate the possible involvement of BPA-induced senescence mechanisms in endothelial cells. The β-Gal assays showed interesting differences in cell senescence at relatively low doses (100 nM and 5 µM). Western blots confirmed that proteins involved in senescence mechanisms, p16 and p21, were overexpressed in the presence of BPA. In addition, the UPR (unfolding protein response) system, which is part of the senescent phenotype, was also explored by Western blot and qPCR, confirming the involvement of the PERK-ATF4-CHOP pathway (related to pathological processes). The endothelium of mice treated with BPA showed an evident increase in the expression of the proteins p16, p21, and CHOP, confirming the results observed in cells. Our results demonstrate that oxidative stress induced by BPA leads to UPR activation and senescence since pretreatment with N-acetylcysteine (NAC) in BPA-treated cells reduced the percentage of senescent cells prevented the overexpression of proteins related to BPA-induced senescence and reduced the activation of the UPR system. The results suggest that BPA participates actively in accelerated cell aging mechanisms, affecting the vascular endothelium and promoting cardiovascular diseases.
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Registered trials
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