Патогенетичні механізми розвитку кардіофіброзу при фібриляції передсердь

The study of the pathogenesis and pathomorphology of cardiofibrosis can be reffered to one of the important problems in modern cardiology. This review paper presents data on the different stages of development of cardiofibrosis in atrial fibrillation (AF). Its significant advantage lies in the study of the molecular mechanisms of the occurrence of the disease from its initial to its final stages. It has been established that a number of activated intracellular signaling pathways and profibrotic factors play a significant role in the pathogenesis of cardiofibrosis. Their interaction leads to the induction and progression of this pathological process. This work also includes consistent and detailed analysis of cytological aspects of cardiofibrosis development in AF. Important conditions that cause the activation of fibroblasts and the acceleration of the fibrotic process are changes in the state of connective tissue cells, cardiomyocytes and other types of resident heart cells. They are directly involved in the regulation of gene expression necessary for the synthesis of specific proteins involved in the formation of fibrous tissue in AF. It has been shown that proliferation of the connective tissue matrix, inflammation, development of oxidative stress, necrosis of cardiomyocytes, progression of fibrosis and pathological remodeling are subsequently observed at the stages of structural histopathological changes that follow the period of functional and metabolic disorders in atria in AF. Thus, it should be expected that in the future the results of relevant cardiological studies will create scientific prerequisites for the development of innovative drugs and technologies. This will allow not only to effectively treat patients with AF, but also influence processes of its development and the formation of heart failure.