BRD4770 functions as a novel ferroptosis inhibitor to protect against aortic dissection

This study explores the role of ferroptosis, a novel iron-dependent regulated cell death driven by excessive lipid peroxidation, in the pathogenesis of aortic dissection (AD). Specifically, we investigated whether targeting ferroptosis could serve as an effective approach for preventing smooth muscle cell (SMC) loss and treating AD. Our findings revealed increased iron levels, ferroptosis-related molecules (TFR, HOMX1, ferritin), and lipid peroxidation product 4-hydroxynonenal in the aorta of AD models.Experimental Design: Human aortic smooth muscle cells (SMCs) were subjected to various interventions to induce ferroptosis and examine the protective effects of BRD4770, an inhibitor of histone methyltransferases. The experimental groups included: DMSO control group, Imidazole ketone erastin group, Imidazole ketone erastin + BRD4770 group, Cystine deprivation group,Cystine deprivation + BRD4770 group. RNA sequencing (RNA-seq) was performed on these groups to analyze gene expression changes.