DCAF7 enhances atherosclerosis in vascular endothelial cells by promoting SLC40A1 transcription through facilitating TNF-mediated NF-κB function

Atherosclerosis (AS) poses a significant risk to human health. Our study, through the analysis of publicly available datasets, discovered that apoptosis plays a crucial role in the development of atherosclerosis. Additionally, we found that the iron apoptosis factor SLC40A1 is greatly increased, while the up-regulation of DCAF7 may be a significant contributing element to this impact. Therefore, we conducted tests both in vivo and in vitro to show that DCAF7 has the ability to influence the expression of SLC40A1 by impacting TNF and controlling the function of NF-κB, resulting in apoptosis. Following the creation of ApoE-/- mice, we suppressed the activity of DCAF7 and observed a substantial reduction in the advancement of carotid atherosclerosis and apoptosis in these animals. This suggests that DCAF7 plays a crucial role in the development of carotid atherosclerosis. Targeting DCAF7 has the potential to halt the progression of atherosclerosis.