Vessel occlusion by rupture or atheroma erosion leading to thrombosis is the underlying cause of severe complications, including sudden cardiac death, myocardial infarction, and stroke. Tissue factor is known to play the key role in the initiation of the majority of stages of coagulation cascade. Recent studies explained the structure, synthesis and activation mechanisms of tissue factor. Tissue factor is the main component of atherothrombotic process and is associated with the immune inflammation, endothelial dysfunction, angiogenesis, and cell migration that play an important role in the development of cardiovascular, inflammatory and oncological pathology. Basal activity of tissue factor is the independent parameter of cardiovascular risk, the predictor of thrombolysis efficacy and affects the results of angioplasty interventions. The effects of medications (e.g. statins), including those in drug-eluting stents, on tissue factor are the objective of further investigation. Studies of physiological and pathogenic role of tissue factor will have a great impact on our understanding of cardiovascular pathology and other diseases.
Peroxisome proliferator receptors alpha (PPAR-α) and their role in atherogenesis has a great practical significance, since there are drugs that can enhance the activity of these receptors. Activation of PPAR-α by fibrates is known to lead to both significant reduction of serum triglyceride levels by activation of lipoprotein lipase, and to the increase of synthesis of the main apolipoproteins within high-density lipoproteins (HDL), contributing to the reverse transport of cholesterol from chylomicrons and very low-density lipoproteins to the liver. Besides, PPAR-α increase the capture of HDL by liver. PPAR-α also participate in the regulation of inflammation, expression of adhesive molecules, production of chemotactic factors, as well as inhibit the proliferation of smooth muscle cells and activity of fibroblasts. These data suggest that PPAR-α are directly involved in the processes of atherogenesis, and their activation may contribute to the regression of atherosclerotic plaque and significant reduction of cardiometabolic risk.
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