FN1-associated cavernous endothelial remodeling induced by bisphenol A: relevance to erectile dysfunction and attenuation by baicalin
Previous studies suggest that bisphenol A (BPA) exposure may impair erectile function, but the underlying cavernous endothelial mechanisms remain unclear. Whether BPA induces endothelial alterations resembling those in d
Erectile dysfunction (ED) is a complex condition affecting millions of men worldwide. Recent studies have suggested that bisphenol A (BPA), a widely used chemical, may contribute to the development of ED by impairing cavernous endothelial function. However, the underlying mechanisms remain poorly understood. This study aimed to investigate the effects of BPA on cavernous endothelial remodeling and its potential link to ED.
The researchers integrated data from previous studies to identify candidate genes involved in BPA-induced endothelial alterations. They found that fibronectin type 1 (FN1), a protein involved in cell adhesion and migration, was consistently prioritized by network topology and machine-learning analyses as a key player in BPA-related endothelial remodeling.
In vitro experiments were conducted using immortalized rat corpus cavernosum endothelial cells to investigate the effects of BPA on FN1 expression, endothelial markers, and signaling pathways. The results showed that BPA increased FN1 expression, reduced endothelial markers, and suppressed PI3K/AKT/eNOS phosphorylation, leading to enhanced mesenchymal-related marker expression and decreased cell viability.
The researchers also found that FN1 knockdown and delayed intervention with baicalin, a natural compound known for its anti-inflammatory properties, partially restored endothelial markers, signaling activity, and cell viability. These findings suggest that FN1-associated endothelial remodeling may represent one component of BPA-related endothelial injury relevant to ED, while baicalin may provide partial protection.
The study highlights the importance of understanding the mechanisms underlying BPA-induced endothelial dysfunction and its potential link to ED. Further research is needed to fully elucidate the role of FN1 in this process and to explore the therapeutic potential of baicalin for preventing or treating ED.
Research-use only: This study was conducted using laboratory peptides and should not be used for clinical purposes without further validation and regulatory approval.