Microcirculatory inflammation in chronic venous insufficiency: current status and future directions.
One of the hallmarks of chronic venous insufficiency (CVI) is an elevated venous pressure. However, no direct link at the cellular and molecular levels between venous hypertension and actual tissue damage in CVI has been established. Evidence for generations of an inflammatory reaction and several molecular alterations in the development of CVI is discussed. Development of experimental models of CVI, analysis of the mechanical tissue stresses in addition to venous hypertension, in combination with systematic studies of clinically stratified and standardized patient-derived samples is required for molecular description of the pathogenesis of CVI.
Durán
W
W
Department of Pharmacology and Physiology, New Jersey Medical School, University of Medicine & Dentistry of New Jersey, Newark, USA.
Pappas
P J
PJ
Schmid-Schönbein
G W
GW
D002908:Chronic Disease; D004730:Endothelium, Vascular / Q000473:pathology / Q000648:ultrastructure; D006801:Humans; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology; D007249:Inflammation / Q000097:blood / Q000473:pathology* / Q000503:physiopathology; D008833:Microcirculation / Q000473:pathology* / Q000503:physiopathology; D013314:Stress, Mechanical; D014689:Venous Insufficiency / Q000097:blood / Q000473:pathology* / Q000503:physiopathology*