Role of mast cells in the pathogenesis of atherosclerosis

Abstract Atherosclerosis is chronic, inflammatory disease. In artery inflammation main role play cells of the immune system, including lymphocytes and macrophages. This circle of the cells modulating atherogenesis enclose also mast cells. Activated mast cell degranulate and release many types of mediators, including cytokines, chemokins, growth factors, vasoactive substances and proteolytic enzymes. This mediators can modulate inflammatory reaction in artery wall directly, by releasing proinflammatory cytokines or indirectly, influencing the activity of the other cells of the immune system, taking a part in the process of atherogenesis. Due to the ability of secretion and activation of proteolytic enzymes (chymase, tryptase, metalloproteinases), mast cells are prone to degrade various components of pericellular and extracellular matrices, including collagen, main protein of the fibrous cap of atherosclerotic plaque, rendering to plaque destabilization, increasing the onset of the atherothrombotic complications. Mast cell proteases can also modulate proliferation and apoptosis of the endothelial and smooth muscle cells of the artery wall. In spite of the fact, that most of the studies about mast cells are performed ex vivo on human tissues or cell cultures and rodents, this findings lead to recognize mechanisms by which mast cell can intervene in atherogenesis process. Moreover, there are some trials of using some of the mast cell mediators in differentiation of cardiovascular diseases and prediction the clinical condition of the patients.