Dermal pathology, cellular biology, and inflammation in chronic venous disease.
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.
Raffetto
Joseph D
JD
Vascular Surgery Division VA Boston Healthcare System, West Roxbury, MA, USA. joseph.raffetto@med.va.gov
D000818:Animals; D049109:Cell Proliferation; D002908:Chronic Disease; D005109:Extracellular Matrix / Q000378:metabolism; D005347:Fibroblasts / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000276:immunology / Q000473:pathology; D007962:Leukocytes / Q000276:immunology; D020782:Matrix Metalloproteinases / Q000378:metabolism; D012307:Risk Factors; D012867:Skin / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D014647:Varicose Ulcer / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D014689:Venous Insufficiency / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology
D053773:Transforming Growth Factor beta1; D020782:Matrix Metalloproteinases