Bisphenol A and Its Substitutes Show Proatherosclerotic Potential through the Dysregulation of CD36-Driven Cholesterol Homeostasis

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.