Inflammation as a therapeutic target in myocardial infarction: learning from past failures to meet future challenges

摘要: In the infarcted myocardium, necrotic cardiomyocytes release danger signals, activating an intense inflammatory response. Inflammatory pathways play a crucial role in regulation of wide range cellular processes involved injury, repair, and remodeling heart. Proinflammatory cytokines, such as tumor necrosis factor α interleukin 1, are markedly upregulated myocardium promote adhesive interactions between endothelial cells leukocytes by stimulating chemokine adhesion molecule expression. Distinct pairs chemokines receptors implicated recruitment various leukocyte subpopulations myocardium. For more than past 30 years, extensive experimental work has explored signals contributions myocardial infarction. Robust evidence derived from models infarction identified targets that may attenuate cardiomyocyte injury or protect adverse remodeling. Unfortunately, attempts to translate promising findings clinical therapy have failed. This review article discusses biology response after infarction, identify causes for translational failures past, proposes new therapeutic directions. Because their potential involvement injurious, reparative, regenerative responses, hold key design therapies