Pocock Elizabeth S, Alsaigh Tom, Mazor Rafi, Schmid-Schönbein Geert W
Department of Bioengineering, The Institute for Engineering in Medicine, University of California San Diego, 92093-0412 La Jolla, California.
Vasc Cell. 2014 Dec 12;6(1):24. doi: 10.1186/s13221-014-0024-5. eCollection 2014.
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.
慢性静脉疾病（CVD）有一系列临床表现，包括下肢静脉迂曲、扩张，皮肤色素沉着增加，严重时受累皮肤会发生溃疡。静脉功能不全是CVD的先兆，其特征是下肢血液回流至心脏不当，必须在能够对人类采取预防措施的最早阶段对其进行研究。这凸显了对影响静脉疾病进展的生物标志物和遗传易感性因素进行基础研究的必要性。过去十年的研究已经深入了解了静脉疾病发生发展背后的这些特定遗传、细胞和分子机制。众多进展包括阐明基质金属蛋白酶在与静脉功能不全相关的退行性过程中作为重要介质的作用日益增强。这可能之前存在一个炎症过程，该过程进一步导致疾病晚期出现的小静脉退变和内皮功能障碍。此外，基因组分析揭示了患病组织样本中基质重塑蛋白的时间表达模式。在这篇综述中，我们研究了目前在阐明慢性静脉疾病病因方面围绕细胞、分子和遗传进展的一些发现。
