Abdominal aortic aneurysms (AAAs) are a chronic degenerative disease with life-threatening implications. While AAAs are thought to arise through a localized form of arterial wall injury superimposed on various predisposing factors, their natural history is one of progressive structural deterioration, gradual expansion, and eventual rupture. Pathologic processes contributing to the changes observed in AAAs include chronic inflammation, destructive remodeling of the extracellular matrix, and depletion of vascular smooth muscle cells. These changes result in progressive aortic dilatation accompanied by alterations in vessel geometry, redistribution of hemodynamic wall stresses, and diminished tensile strength. As outlined in this review, better understanding of the biological mechanisms underlying these changes will allow design of novel therapeutic strategies to suppress the process of aneurysmal degeneration.