Molecular Pathways for Progression of Myocardial Fibrosis. Potentials of Therapy

INTRODUCTION: Myocardial fibrosis underlies the development of rhythm disturbances. It is the main component that promotes progression of many diseases, in particular, remodeling of the myocardium and the vessel wall. Besides, the data are being accumulated in the literature about the influence of intercellular interaction factors on remodeling of heart chambers. Fibrotic tissue isolates the groups of atrial cardiac myocytes, as well as individual cells, thereby disrupting connections between them and slowing down the conduction velocity, which is the cause of rhythm disorders leading to the development of atrial fibrillation. Fibrotic changes underlie many diseases, which suggests their common pathogenic pathways. These pathways are realized through complex activity within different cells, in which specific molecular pathways arise. Apart from many cells involved in the response to injury, of decisive significance are the main molecular pathways. As fibrosis progresses, the myofibroblasts proliferate and sense physical and biochemical stimuli via integrins and other molecules, while contractile mediators induce pathological tissue contraction. This chain of events, in turn, causes organ deformation that impairs its function. Thus, the biology of fibrogenesis is dynamic, although the degree of plasticity is likely to vary from organ to organ. CONCLUSION: The organ injury results in activation of the immune system and release of proinflammatory cytokines from cells. Proinflammatory cytokines contribute to dysfunction of cardiac myocytes, proliferation and deposition of collagen, initiation and progression of fibrosis. Attempts to treat patients with drugs inhibiting proinflammatory cytokines have been used in relation to fibrosis of the liver and lungs. Studies of the use of these drugs in relation to the myocardium have not been conducted to date. Therefore, investigation of new ways of immune correction to improve antifibrotic therapy in relation to the myocardium is an urgent task at present.