Journal
CARDIOVASCULAR RESEARCH
Volume 75, Issue 4, Pages 640-648Publisher
OXFORD UNIV PRESS
DOI: 10.1016/j.cardiores.2007.06.023
Keywords
adventitia; vascular inflammation; fibroblast; myofibroblast; lymphocytes
Categories
Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL090584, R01HL070531, P01HL058000] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK059499] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01 HL070531-07, HL58000, R01 HL090584, R01 HL090584-04, HL70531, R01 HL070531] Funding Source: Medline
- NIDDK NIH HHS [R01 DK059499, R01 DK059499-04] Funding Source: Medline
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Traditional concepts of vascular inflammation are considered inside-out responses centered on the monocyte adhesion and lipid oxidation hypotheses. These mechanisms likely operate in concert, holding the central tenet that the inflammatory response is initiated at the luminal surface. However, growing evidence supports a new paradigm of an outside-in hypothesis, in which vascular inflammation is initiated in the adventitia and progresses inward toward the intima. Hallmarks of the outside-in hypothesis include population of the adventitia with exogenous cell types, including monocytes, macrophages, and lymphocytes, the phenotypic switch of adventitial fibroblasts into migratory myofibroblasts, and increased vasa vasorum neovascularization. The resident and migrating cells deposit collagen and matrix components, respond to and upregulate inflammatory chemokines and/or antigens, and regulate the local redox state of the adventitia. B cells and T cells generate local humoral immune responses against local antigen presentation by foam cells and antigen presenting cells. These events result in increased local expression of cytokines and growth factors, evoking an inflammatory response that propagates inward toward the intima. Ultimately, it appears that the basic mechanisms of cellular activation and migration in vascular inflammation are highly conserved across a variety of cardiovascular disease states and that major inflammatory events begin in the adventitia.
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