Abstract
An abdominal aortic aneurysm (AAA) is defined as a localized dilation of the abdominal aorta measuring at least 1.5 times its normal diameter. If left untreated, AAA can progress to a life-threatening condition. In the field of AAA, treatment strategies have evolved significantly, with endovascular aneurysm repair serving as a representative example. However, despite developments in surgical techniques, postoperative morbidity and mortality rates remain significant. Extensive research is being conducted to examine the genetic and environmental risk factors of AAA to better understand its pathophysiology and develop novel therapeutic or preventive strategies. Numerous genome-wide association studies have identified factors associated with AAA progression, including mechanisms involving lipid metabolism. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is important in abnormal lipid metabolism because it regulates low-density lipoprotein levels. PCSK9 also inhibits the proliferation of human aortic smooth muscle cells (SMCs). Loss of SMCs due to PCSK9-induced apoptosis can lead to thinning of the fibrous cap and contribute to plaque vulnerability and degeneration of the medial layer. PCSK9 inhibitors are widely used in clinical practice, particularly in cardiovascular diseases. The aim of this study was to elucidate the genetic pathophysiology of AAA and explore how PCSK9 can be utilized for the prevention and treatment of AAA.