Targeting Chemokines in Aortic Aneurysm

Abstract

Aortic aneurysm rupture and aortic dissection are important causes of death. In the last decade, several developments have improved the outlook for patients with aortic diseases, including the introduction of ultrasound screening for abdominal aortic aneurysm (AAA) in some countries; more detailed ways of imaging the aorta and the development and subsequent sophisticated advancement of technology to repair large aortic aneurysms via endovascular means. An important remaining challenge is the development of an effective range of medications, which limit the progression of aortic aneurysms and dissections.1 See accompanying article on page 718 Although the molecular biological characteristics of aortic aneurysms vary depending on the region of the aorta affected and the risk profile of the patient, a key pathological feature is inflammation. Biopsies of human AAA wall and thrombus have been shown to be densely infiltrated by a range of innate and adaptive immune cells, including neutrophils, macrophages, mast cells, lymphocytes, and dendritic cells.2 Studies in rodent models suggest that blocking aortic wall inflammation can limit the development and progression of aortic aneurysm.3 Currently, however, no effective and safe means of limiting aneurysm progression in patients has been developed.1 Chemokines are a group of structurally related cytokines originally defined by their ability to promote cell migration, especially that of inflammatory cells. Previous studies have demonstrated upregulation of a range of different chemokines within animal models of aortic aneurysm and human …