mouse model, BPs exposure increased aortic plaque burden. These effects were significantly reduced or eliminated in CD36-silenced cells and mice. Interestingly, BPA substitutes exhibited more potent effects than BPA itself. Molecular docking further supported the direct interaction between BPs and CD36, as well as the structure-toxicity relationship trend of these BPs. Overall, the findings suggest that BPs promote CD36-mediated lipid accumulation and the development of atherosclerosis. The study highlights the need to reevaluate the safety of BPs and provides a foundation for risk assessment and prevention strategies related to BPs exposure and cardiovascular disease.
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Yang et al. (Thu,) studied this question.
www.synapsesocial.com/papers/69f6e5f38071d4f1bdfc68fc — DOI: https://doi.org/10.1021/acs.est.5c18707
B Yang
Xiangyu Zhu
T R Sun
Chinese Academy of Sciences
University of Chinese Academy of Sciences
Beijing Normal University
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