PPARGC1A and atherosclerosis: KCa3.1 silencing leads to alterations in key nuclear factors, including downregulation of cfos and NR4A1 and upregulation of PPARα, PPARγ, and PGC1α (1.8-fold, p < 0.05) subsequently predicted to lead to inhibition of key atherogenic processes including leukocyte infiltration, macrophage activation, SMC proliferation, and necrosis, resulting in inhibition of atherosclerosis observed in the current experiment.