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Aortic aneurysms and aortic dissections account for ~16,000 deaths in the United States annually (Kuivaniemi, et al., 2008). Recent evidence suggests that enhanced vascular inflammation underlies the progression of both abdominal aortic aneurysms and thoracic aortic aneurysms (Guo, et al., 2006a). Common pathologic features of vascular inflammation and aneurysmal disease include recruitment and activation of immune cells to the vessel wall, myofibroblast differentiation and extracellular matrix (ECM) remodeling. Recent preclinical work has implicated divergent signaling pathways downstream of the vasopressor angiotensin II (Ang II) peptide in controlling these activities. This work has elucidated two important paracrine signaling networks, one mediated by the NF-κB-IL-6 pathway controlling monocyte activation, and the second mediated by the TGF-β-Smad2 pathway controlling myofibroblast differentiation and T lymphocyte differentiation. Antagonism of Ang II signaling is being evaluated in the clinical management of patients with familial thoracic aneurysms. In this chapter, we will review the multifaceted role of Ang II in vascular inflammation in aortic aneurysmal disease.

Multifaceted Role of Angiotensin II in Vascular Inflammation and Aortic Aneurysmal Disease