Abstract
Varicose veins are superficial vessels that are abnormally twisted, lengthened, or dilated, and they are usually caused by inefficient or defective valves within the vein. Varicose veins are part of the spectrum of chronic venous diseases (CVDs), which affect millions of people throughout Western populations [1]. There is significant evidence in the literature that wall dysfunction consisting of alterations in the endothelium and smooth muscle cells (SMCs) are a principal cause for varicose veins [2]. In addition, matrix metalloproteinases (MMPs) are present in varicose veins and can be found in the endothelium, smooth muscle, and adventitial layers of the vein wall [3]. However, it is unclear whether the presence of MMPs is a result of chronic inflammation and venous wall remodeling or whether MMPs actually functional in veins, causing biochemical changes in the venous wall, leading to early dilation and chronic irreversible changes typified by varicose veins [2]. Furthermore, the role of venous wall dysfunction appears to precede valve dysfunction, is linked to MMPs [2], and is tightly regulated by hypoxia inducible factor.
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Raffetto, J.D. (2013). Varicose Veins: Venous Wall Changes, Inflammation, and Matrix Metalloproteinases. In: Gabriel, E., Gabriel, S. (eds) Inflammatory Response in Cardiovascular Surgery. Springer, London. https://doi.org/10.1007/978-1-4471-4429-8_22
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DOI: https://doi.org/10.1007/978-1-4471-4429-8_22
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