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The present review considers current data on the structure, functions and role of interleukin-13 in the pathogenesis of vascular wall varicose transformation in terms of proteolysis and inflammatory response. It is known that interleukin-13 is able to interact with transforming growth factor-1 in diseases associated with fibrosis. The latter activates fibroblasts and excessive formation of the extracellular matrix, thereby inducing fibrosis of the vascular wall, which is one of the links in the pathogenesis of varicose veins. Also, to date, there is evidence of the interleukin-13 participation in the induction of certain proteolytic enzymes synthesis, such as matrix metalloproteinases. For the latter, participation in the transformation of the venous wall has been proven to date. The remodeling of the venous wall itself can lead to an increase in the expression of proteinases, providing a proteolytic mechanism for changing the structural organization of the venous wall in varicose veins of the lower extremities. At the same time, the involvement of lysosomal cysteine proteinases remains poorly understood. The expression and production of individual cathepsins are regulated by biologically active molecules: interleukin-1, interleukin-6, tumor necrosis factor , which are directly involved in inflammatory reactions in the wall of varicose veins. In particular, venous pathology develops in a vicious circle of inflammation with the formation of abnormal venous blood flow, chronic venous hypertension and dilation, and the recruitment of leukocytes. This leads to a further, deeper, remodeling of the walls and valves of the veins, an increase in blood pressure and the release of pro-inflammatory mediators chemokines and cytokines. In connection with the above, in order to understand the mechanisms of proteolysis in the vascular wall in varicose veins of the lower extremities, it is important to have an idea about the possible interactions of interleukin-13 with transforming growth factor-1, inflammatory cytokines, and cathepsins.
The present review considers current data on the structure, functions and role of interleukin-13 in the pathogenesis of vascular wall varicose transformation in terms of proteolysis and inflammatory response. It is known that interleukin-13 is able to interact with transforming growth factor-1 in diseases associated with fibrosis. The latter activates fibroblasts and excessive formation of the extracellular matrix, thereby inducing fibrosis of the vascular wall, which is one of the links in the pathogenesis of varicose veins. Also, to date, there is evidence of the interleukin-13 participation in the induction of certain proteolytic enzymes synthesis, such as matrix metalloproteinases. For the latter, participation in the transformation of the venous wall has been proven to date. The remodeling of the venous wall itself can lead to an increase in the expression of proteinases, providing a proteolytic mechanism for changing the structural organization of the venous wall in varicose veins of the lower extremities. At the same time, the involvement of lysosomal cysteine proteinases remains poorly understood. The expression and production of individual cathepsins are regulated by biologically active molecules: interleukin-1, interleukin-6, tumor necrosis factor , which are directly involved in inflammatory reactions in the wall of varicose veins. In particular, venous pathology develops in a vicious circle of inflammation with the formation of abnormal venous blood flow, chronic venous hypertension and dilation, and the recruitment of leukocytes. This leads to a further, deeper, remodeling of the walls and valves of the veins, an increase in blood pressure and the release of pro-inflammatory mediators chemokines and cytokines. In connection with the above, in order to understand the mechanisms of proteolysis in the vascular wall in varicose veins of the lower extremities, it is important to have an idea about the possible interactions of interleukin-13 with transforming growth factor-1, inflammatory cytokines, and cathepsins.
INTRODUCTION: The binary in-stent restenosis (ISR) still remains the main factor limiting the effectiveness of percutaneous coronary intervention in the long-term period. Histologically, ISR is defined as neointimal hyperplasia leading to hemodynamically significant narrowing of the arterial lumen. Patients with coronary artery (CA) restenosis represent a particularly challenging group for endovascular treatment. AIM: To compare effectiveness and safety of the endovascular correction of coronary in-stent restenosis using second- and third-generation stent systems and balloon angioplasty with a drug-coated balloon catheter. MATERIALS AND METHODS: The study retrospectively included 62 patients with recurrent ISR after the previous endovascular correction. The patients underwent treatment with re-stenting in Saint George Clinic of Thoracic and Cardiovascular Surgery of the National Pirogov Medical Surgical Center in 2016–2023 with use of second- and third-generation drug-eluting stents — cobalt (cobalt alloy) systems with zotarolimus, cobalt-chromium stent systems with sirolimus and zotarolimus, platinum-chromium stent systems with everolimus with biodegradable drug coating. Balloon angioplasty was performed using paclitaxel-coated balloon catheters. The primary endpoint of the study was the target lesion failure (TLF) of CA. The secondary endpoint was major adverse cardiovascular events (MACE). RESULTS: The TLF rate was 15.6% vs. 13.3% and 28.1% vs. 46.7% in the groups with use of a drug-eluting stent and balloon angioplasty at 1- and 2-year follow-up, respectively (p = 0.30). MACE was recorded in 18.8% vs. 16.7% and 37.5% vs. 56.7% of cases in the groups with use of a drug-eluting stent and balloon angioplasty at 1- and 2-year follow-up, respectively (p = 0.25). The dispersion analysis of predictors of TFL risks identified three factors showing a reliable correlation with the probability for TFL by the second follow-up year in both groups: (1) recurrence of binary ISR (hazard ratio (HR) 2.21; 95% confidence interval (CI) 0.95–4.01; p = 0.03)) in 365 days after the third stage of the percutaneous coronary intervention; (2) length of coronary restenotic lesion (per every 10 mm) (HR 1.25; 95% CI 0.99–1.40; p = 0.002); (3) occlusive restenosis (HR 4.16; 95% CI 0.43–26.96; p = 0.04). CONCLUSIONS: The implantation of a second- and third-generation drug-eluting stent and balloon angioplasty with use of a drug-coated catheter are comparable in the effectiveness and safety in correcting the recurrent ISR, however, restenting is associated with a lower probability for developing TFL and adverse events.
The review considers the involvement of the endothelium and endothelial glycocalyx in the systemic inflammatory response. The role of the endothelium in the inflammation is ambivalent and depends on the nature of the inflammatory process. The physiological response of endothelial cells to local inflammation is necessary to successful eliminate the pathogen and restore the tissue homeostasis. In systemic inflammation, the endothelium is the most «suffering» structure of the body. However, endothelial cells can be a source of systemic inflammatory mediators, supporting the pathological inflammatory process. The problem of generalization of inflammation is discussed where endotheliopathy develops and closes the vicious circle, being both a consequence of systemic inflammation and the cause of its prolongation and intensification. In the pathogenesis of a new coronavirus infection the relationship between endotheliopathy and systemic inflammation was most clearly manifested. Preceding endothelial dysfunction causes a severe course of COVID-19 with a «cytokine storm» and coagulopathy that can lead to the death. SARS-CoV-2 infection induces long-term endothelial dysfunction, which is recorded even after the virus elimination. The early detection of blood level of endothelial glycocalyx damage markers (i. e. syndecan-1, glycosaminoglycans like heparan sulfate and hyaluronic acid) may seem to be an effective approach to the prevention of severe forms of COVID-19. Endothelial-protective drugs can reduce the risk of severe new coronavirus infection and eliminate the manifestations of long-COVID.
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