Extracellular matrix, inflammation, and the angiogenic response

Inflammation and angiogenesis are frequently coupled in pathological situations such as atherosclerosis, diabetes, and arthritis. The inflammatory response increases capillary permeability and induces endothelial activation, which, when persistent, results in capillary sprouting. This inflammation-i...

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Bibliographic Details
Published in:Cardiovascular research 2010-05, Vol.86 (2), p.226-235
Main Authors: Arroyo, Alicia G., Iruela-Arispe, M. Luisa
Format: Article
Language:English
Subjects:
Angiogenesis
Animals
Capillary Permeability
Endothelium, Vascular - immunology
Endothelium, Vascular - physiopathology
Extracellular matrix
Extracellular Matrix - immunology
Growth factors
Humans
Inflammation
Inflammation - immunology
Inflammation - physiopathology
Neovascularization, Pathologic - immunology
Neovascularization, Pathologic - physiopathology
Neovascularization, Physiologic
Proteases
Signal Transduction
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Summary:Inflammation and angiogenesis are frequently coupled in pathological situations such as atherosclerosis, diabetes, and arthritis. The inflammatory response increases capillary permeability and induces endothelial activation, which, when persistent, results in capillary sprouting. This inflammation-induced angiogenesis and the subsequent remodelling steps are in large part mediated by extracellular matrix (ECM) proteins and proteases. The focal increase in capillary permeability is an early consequence of inflammation, and results in the deposition of a provisional fibrin matrix. Subsequently, ECM turnover by proteases permits an invasive program by specialized endothelial cells whose phenotype can be regulated by inflammatory stimuli. ECM activity also provides specific mechanical forces, exposes cryptic adhesion sites, and releases biologically active fragments (matrikines) and matrix-sequestered growth factors, all of which are critical for vascular morphogenesis. Further matrix remodelling and vascular regression contribute to the resolution of the inflammatory response and facilitate tissue repair.
ISSN:0008-6363
1755-3245
DOI:10.1093/cvr/cvq049