Exact mechanisms of varicose veins are still unclear and actively studied by clinicians and scientists. Vein wall transformation is a result of remodeling processes that are triggered by the so-called vein-specific inflammation. This chronic process involves a complex of interactions between the cells responsible for inflammatory response (neutrophils, lymphocytes, monocytes, macrophages), endothelial cells, vascular smooth muscle cells and extracellular matrix. In addition, vein-specific inflammation occurs with active participation of cytokines. These are a diverse group of small proteins released by different immune and vascular cells in picomolar and nanomolar concentrations. Cytokines activate specific receptors and modulate the functions of various cells and tissues. The role of cytokines in pathogenesis of varicose veins remains poorly understood due to difficult research of their mechanism of action. It is assumed that their activity mediates impaired regulation of degradation processes in extracellular matrix, modification of the components of extracellular matrix (collagen and elastin) and decrease in the number of smooth muscle cells. All these processes reduce an efficiency of vascular wall contraction due to fragmentation of the muscle layer. Cytokines are also involved in activation of leukocytes that results a release of free radicals, activation of proteases and subsequent degradation of smooth muscle cells. In this review, we analyzed various data on cytokines and studies devoted to possible impact of various molecules on development of primary varicose veins.