Nuclear factor kappa B as a potential target for pharmacological correction endothelium-associated pathology

Abstract

The nuclear factor kappa B (NF-κB) is one of transcription factors. A high interest in   studying the biological role of the signal system and its contribution to the development of   cardiovascular, oncological and autoimmune diseases is obvious. A number of stimuli (proinflammatory   cytokines: tumor necrosis factor α, interleukin 1β, ligand CD40 and others) trigger   the canonical and non-canonical pathways of NF-κB signaling, which increase the expression of   genes regulating synthesis of cytokines and chemokines, cell proliferation and differentiation,   angiogenesis, immune reactions and apoptosis. However, pathological activation of NF-κB   violates the balance of substances participating in the normal activity of the cardiovascular   system. This leads to the development and progression of endothelium-associated pathology and   comorbidity. Contribution of pathological activation the NF-κB signaling system in the formation   of vicious circles in atherosclerosis, coronary heart disease, pulmonary hypertension, ischemicreperfusion   injury, is not subject to doubt. Thus, the search for new therapeutic targets and   strategies for modulating the activity of the NF-κB signaling pathway is one of the key strategies   for the development of experimental pharmacology. Another important aspect of studying the   pharmacological activity of NF-κB activity modulators is the choice of a valid and easily   reproducible way of assessing the activity of this system.