Cellular and molecular mechanisms of inflammation in pathogenesis of myocardial infarction
There is increasing evidence showing that inflammation accounts for myocardial infarction progression. This review summarizes our current understanding of the cellular and molecular mechanisms regulating the inflammatory response following myocardial ischemia. Myocardial necrosis induces complement activation, triggering a cytokine cascade. Inflammation is characterized by the accumulation of inflammatory cells (leukocytes, macrophages) in the ischemic myocardial. Сells infiltration is regulated through the complex sequence of molecular steps involving selectins and integrins, which mediate leukocyte rolling and adhesion to the endothelium. Once activated, inflammatory cells can release a variety of cytotoxic agents including more cytokines and matrix metalloproteinases.