Published online before print March 29, 2007, doi: 10.1161/ATVBAHA.106.137851
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© 2007 American Heart Association, Inc.
Brief Reviews |
Topological Determinants and Consequences of Adventitial Responses to Arterial Wall Injury
From the Institut National de la Sante et de la Recherche Medicale (INSERM) Unit 698 and University Denis Diderot-Paris 7 (J.-B.M, X.H., O.M.), CHU Xavier Bichat, Paris, France; and the INSERM Uníte Mixte de Recherches 681 (O.T., G.C., A.N.), Université Pierre et Marie Curie-Paris 6, Centre de recherche des Cordeliers, Paris, France.
Correspondence to Jean-Baptiste Michel, MD, PhD, INSERM unit 698, Cardiovascular hematology, bio-engineering & remodeling, CHU Xavier Bichat, 46 rue Henri Huchard, 75018 Paris, France. E-mail jbmichel{at}bichat.inserm.fr
Arteries are composed of 3 concentric tissue layers which exhibit different structures and properties. Because arterial injury is generally initiated at the interface with circulating blood, most studies performed to unravel the mechanisms involved in injury-induced arterial responses have focused on the innermost layer (intima) rather than on the outermost adventitial layer. In the present review, we focus on the involvement of the adventitia in response to various types of arterial injury leading to vascular remodeling. Physiologically, soluble vascular mediators are centrifugally conveyed by mass transport toward the adventitia. Moreover, in pathological conditions, neomediators and antigens can be generated within the arterial wall, whose outward conveyance triggers different patterns of local adventitial response. Adventitial angiogenesis, immunoinflammation, and fibrosis sequentially interact and their net balance defines the participation of the adventitial response in arterial pathology. In the present review we discuss 4 pathological entities in which the adventitial response to arterial wall injury participates in arterial wall remodeling. Hence, the adventitial adaptive immune response predominates in chronic rejection. Inflammatory phagocytic cell recruitment and initiation of a shift from innate to adaptive immunity characterize the adventitial response to products of proteolysis in abdominal aortic aneurysm. Adventitial sprouting of neovessels, leading to intraplaque hemorrhages, predominates in atherothrombosis. Adventitial fibrosis characterizes the response to mechanical stress and is responsible for the constrictive remodeling of arterial segments and initiating interstitial fibrosis in perivascular tissues. These adventitial events, therefore, have an impact not only on the vessel wall biology but also on the surrounding tissue.
The present review focuses on involvement of the adventitia in the response to arterial injury leading to vascular remodeling. The initial luminal insult lead to the genesis of (neo-) mediators that are centrifugally conveyed towards the adventitia. These mediators trigger local adventitial responses including angiogenesis, immuno-inflammation, and fibrosis.
Key Words: mass transport • angiogenesis • lymphoid neogenesis • chronic rejection • abdominal aortic aneurysm • atherothrombosis
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