Topological determinants and consequences of adventitial responses to arterial wall injury.
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.
Michel
Jean-Baptiste
JB
INSERM unit 698 and University Denis Diderot-Paris 7, CHU Xavier Bichat, 46 rue Henri Huchard, 75018 Paris, France. jbmichel@bichat.inserm.fr
Thaunat
Olivier
O
Houard
Xavier
X
Meilhac
Olivier
O
Caligiuri
Giuseppina
G
Nicoletti
Antonino
A
D000818:Animals; D000941:Antigens / Q000378:metabolism; D017544:Aortic Aneurysm, Abdominal / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D001158:Arteries / Q000276:immunology / Q000293:injuries* / Q000378:metabolism / Q000473:pathology / Q000637:transplantation; D050197:Atherosclerosis / Q000378:metabolism / Q000473:pathology*; D003238:Connective Tissue / Q000098:blood supply / Q000276:immunology / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D005355:Fibrosis; D006084:Graft Rejection / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D008221:Lymphoid Tissue / Q000276:immunology / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000473:pathology; D010447:Peptide Hydrolases / Q000378:metabolism; D010586:Phagocytes / Q000276:immunology; D013314:Stress, Mechanical; D017539:Tunica Intima / Q000473:pathology; D017540:Tunica Media / Q000473:pathology
D000941:Antigens; D036341:Intercellular Signaling Peptides and Proteins; D010447:Peptide Hydrolases