Yanfei Yang, Yuhang Liu, Yuexin Chen
Abdominal Aortic Aneurysm (AAA) is characterized by persistent inflammation, extracellular matrix loss, and intraluminal thrombus formation, yet the genetic links among these processes remain incompletely defined. Here, we examine evidence that genetic variation can influence inflammatory and thrombotic responses at the same time. Findings from genome-wide association studies are considered alongside transcriptomic, proteomic, single-cell, epigenetic, and experimental data. Particular attention is given to candidate genes and signaling networks relevant to AAA susceptibility, enlargement, and rupture. The available evidence supports a model in which inherited susceptibility alters the balance between vascular inflammation, coagulation, fibrinolysis, and wall repair. However, many reported loci still lack functional confirmation, and most genetic data come from populations of European ancestry. Defining the causal variants and the cells in which they act will be necessary before these findings can be used for individualized screening or treatment.