Abstract
Cardiovascular diseases continue to be the main cause of hospital mortality and lead to great disability of the working population. Numerous clinical and experimental studies have shown that inflammation is the main factor causing the growth and progression of atherosclerosis. Despite significant progress in basic therapy aimed at both preventing the development of heart failure (HF) and treating it, the prognosis in patients after their first hospitalization remains extremely unfavorable. HF is the leading cause of morbidity and mortality worldwide. Various stimuli at different stages of HF pathophysiology trigger a cascade of proinflammatory reactions with the release of interleukins, the formation of reactive oxygen species, mitochondrial DNA damage and the induction of autophagy. Based on the presented results from experimental and clinical studies, it can be expected that a better understanding of the molecular aspects in the pathophysiology of HF will open opportunities for the development of new therapeutic monoclonal antibodies.