“…Studies have shown that KLF7 expression decreases in oxidized low-density lipoprotein (ox-LDL)-induced HUVECs and inhibiting KLF7 reverses the inhibition effect of miR-301a-3p, promoting inflammation, apoptosis, and oxidative stress in ox-LDL-induced HUVECs [ 55 ]. EGR1, identified as a transcription factor activated by vascular injury, has been implicated in the pathogenesis of various vascular diseases, including AAA, TAA, atherosclerosis, myocardial ischemia/reperfusion injury, hypertension, and pathological angiogenesis [ [56] , [57] , [58] , [59] , [60] , [61] , [62] ]. This underscores the potential of EGR1 regulation as an exploitable target in IAs.…”