Cellular and molecular basis of Venous insufficiency

Vascular Cell

Geert W Schmid-Schönbein¹  Rafi Mazor¹  Tom Alsaigh¹  Elizabeth S Pocock¹ 

[1] Department of Bioengineering, The Institute for Engineering in Medicine, University of California San Diego, La Jolla, 92093-0412, California

关键词: Blood vessel;    Endothelial;    Valves;    Genetics;    Molecular;    Venous disease;    Vein;   

Others  :  1130999
DOI  :  10.1186/s13221-014-0024-5

 received in 2014-10-30, accepted in 2014-11-20,  发布年份 2014

【 摘 要 】

Chronic venous disease (CVD) has a range of clinical presentations, including tortuous, distended veins in lower extremities, increasing skin pigmentation, and in severe cases ulceration of the affected skin. Venous insufficiency, a precursor to CVD characterized by improper return of blood from the lower extremities to the heart, must be studied in its earliest stages at a time when preventative measures could be applied in man. This underscores the need for basic research into biomarkers and genetic predisposing factors affecting the progression of venous disease. Investigation over the past decade has yielded insight into these specific genetic, cellular and molecular mechanisms underlying the development of venous disease. Among the many advances include the elucidation of an increasing role for matrix metalloproteinases as important mediators of the degenerative process involved with venous insufficiency. This may be preceded by an inflammatory process which further contributes to venular degeneration and endothelial dysfunction seen in advanced presentation of disease. Furthermore, genomic analyses have shed light upon temporal expression patterns of matrix remodeling proteins in diseased tissue samples. In this review we examine some of the current findings surrounding cellular, molecular and genetic advances in delineating the etiology of chronic venous disease.

【 授权许可】

   
2014 Pocock et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

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