| Sumario: | Mast cells are recognized effector cells in allergic inflammatory responses. The suggestion that mast cells may participate in the fibrotic process is supported by studies demonstrating that mast cells are capable of producing a wide variety of mediators, such as histamine, tryptase, TNF-a, bFGF, and TGF-b, which can modulate fibroblast phenotypic characteristics and extracellular matrix synthesis. Mast cells and their mediators have been implicated in several disorders involving the human heart. Increased numbers of mast cells have been reported in explanted human hearts with dilated cardiomyopathy and in animal models of experimentally induced hypertension, myocardial infarction, and chronic volume overload secondary to aortocaval fistula and mitral regurgitation. Development of atherosclerosis is associated with participation of various cell types of the immune system such as: granulocytes, B and T lymphocytes, mast cells, dendritic cells and progenitor cells. The presence of mast cells around and within coronary blood vessels suggests that local activation of cardiac mast cells might contribute, through the release of vasoactive mediators, to the pathophysiology of ischemic heart disease. In vitro studies have verified that mast cell proteases are capable of activating collagenase, gelatinases and stromelysin. This review examines: tried to examine the role of mast cells on cardiac diseases.
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