Journal
THROMBOSIS RESEARCH
Volume 123, Issue -, Pages S66-S71Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0049-3848(09)70147-1
Keywords
Venous ulcer; Lipodermatosclerosis; Chronic venous disease; Fibrosis; Inflammation; Leukocyte; Fibroblasts; Growth factors; Matrix metalloproteinase (MMP); Mitogen activated protein kinase (MAPK)
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The pathophysiology of venous dermal pathology in chronic venous disease (CVD) is reflective of a complex interplay that involves sustained venous hypertension, inflammation, cytokine and matrix metalloproteinase (MMP) activation, and altered cellular function. Endothelial expression of specific adhesion molecules recruits (leukocytes, and diapedesis of these cells into the dermal microvasculature promotes an inflammatory response with activation of cytokines and proteinases. Altered cell function enhances a state of vulnerability in the surrounding tissues initiating specific changes associated with venous disease. Ultimately, the persistent inflammatory-proteinase activity leads to advanced chronic venous insufficiency (CVI) and ulcer formation. (C) 2009 Elsevier Ltd. All rights reserved.
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