Mechanical Stretching of Cells of Different Tissues: The Role of Mediators of Innate Immunity

The current review describes the modern conce of how the mechanical stretch (MS) affects cytokine and chemokine production by the cells of different tissues (cardiomyocytes, fibroblasts, smooth muscle cells, endothelial cells and pulmonary cells). Released mediators regulate cell functions such as synthesis of the extracellular matrix proteins, proliferation, apoptosis and others, in autocrine or paracrine manner. Endogenous cytokines (tumor necrosis factor α (TNFα), insulin-like growth factor 1 (IGF-1), vascular endothelial growth factor (VEGF), interleukin 6 (IL-6) and others) produced in myocardium in response to mechanical stretch (MS) may trigger pathological processes resulting in myocyte growth, apotosis and formation of reactive fibrosis. Mechanical load is associated with increase in tissue volume and tissue remodeling. This review provides data about changes in expression of cytokine receptors expression, as well as receptors of innate immunity (TLRs), in response to MS. TLR4 is expressed on the surface of cells of the heart, including cardiomyocytes, smooth muscle cells and endothelial cells. Cyclic MS enhances expression of TLR4 in cultured neonatal rat cardiomyocytes. Excessive MS may result in alterations of cell structure and functions, composition of extracellular matrix (ECM), and promote development of pathological conditions such as hypertrophy, fibrosis, atherosclerosis, osteoporosis, etc. Searching for drugs with targeted action working at the extracellular, membrane and intracellular levels and which will improve the consequences of excessive MS is of undoubted interest and is actual for the treatment of many human pathologies.