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Brief Reviews |
From The Donald W. Reynolds Cardiovascular Clinical Research Center, Cardiovascular Division, Department of Medicine (K.S., P.L.), and Department of Pathology (R.N.M.), Brigham and Womens Hospital, Harvard Medical School, Boston, Mass.
Correspondence to Koichi Shimizu, MD, PhD, Cardiovascular Division, Brigham and Womens Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, NRB7, Boston, MA 02115. E-mail ksmz{at}rics.bwh.harvard.edu
Series Editor: Robert W. Thompson
Abdominal Aortic Aneurysms: Pathophysiological Mechanisms and Clinical Implications
ATVB In Focus
Previous Brief Reviews in this Series:
Powell JT, Brady AR. Detection, management, and prospects for the medical treatment of small abdominal aortic aneurysms. 2004;24:241245.
Daugherty A, Cassis LA. Mouse models of abdominal aortic aneurysms. 2004;24:429434.
Pasterkamp G, Galis ZS, de Kleijn DPV. Expansive arterial remodeling: location, location, location. 2004;24:650657.
Expansion and rupture of abdominal aortic aneurysms (AAA) result in high morbidity and mortality rates. Like stenotic atherosclerotic lesions, AAA accumulate inflammatory cells, but usually exhibit much more extensive medial damage. Leukocyte recruitment and expression of pro-inflammatory Th1 cytokines typically characterize early atherogenesis of any kind, and modulation of inflammatory mediators mutes atheroma formation in mice.1 However, the mechanistic differences between stenotic and aneurysmal manifestations of atherosclerosis remain unexplained. We recently showed that aortic allografts deficient in interferon-
(IFN-
) signaling developed AAA correlating with skewed Th2 cytokine environments, suggesting important regulatory roles for Th1/Th2 cytokine balance in modulating matrix remodeling and important implications for the pathophysiology of aortic aneurysm and atherosclerosis. Further probing of their distinct aspects of immune and inflammatory responses in vascular diseases should continue to shed new light on the pathophysiologic mechanisms that give rise to aneurysmal versus occlusive manifestations and atherosclerosis.
Th1/Th2 cytokine balance plays important regulatory roles in modulating matrix remodeling in vascular diseases. These distinct aspects of immune and inflammatory responses in vascular diseases should continue to shed new light on the pathophysiologic mechanisms that give rise to aneurysmal versus occlusive manifestations and atherosclerosis.
Key Words: aortic aneurysm atherosclerosis cytokine pathogenesis T-lymphocytes transplantation
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