One of the major therapeutic goals of modern cardiology is to design strategies aimed at minimizing @entity296 and optimizing cardiac repair following @entity583 . However, a sound understanding of the biology is necessary before a specific intervention is pursued on a therapeutic basis. This review summarizes our current understanding of the cellular and molecular mechanisms regulating the inflammatory response following @entity741 and reperfusion. @entity296 induces complement activation and free radical generation, triggering a cytokine cascade initiated by Tumor @entity39 Factor (TNF)-alpha release. If reperfusion of the infarcted area is initiated, it is attended by an intense inflammatory reaction. @entity687 synthesis and C5a activation have a crucial role in recruiting neutrophils in the @entity63 and reperfused myocardium. Neutrophil infiltration is regulated through a complex sequence of molecular steps involving the selectins and the integrins, which mediate leukocyte rolling and adhesion to the endothelium. Marginated neutrophils exert potent cytotoxic effects through the release of proteolytic enzymes and the adhesion with Intercellular Adhesion Molecule (ICAM)-1 expressing cardiomyocytes. Despite this potential injury, substantial evidence suggests that reperfusion enhances cardiac repair improving @entity1 survival; this effect may be in part related to the inflammatory response. @entity2842 is also markedly upregulated in the @entity1188 inducing recruitment of mononuclear cells in the injured areas. Monocyte-derived macrophages and mast cells may produce cytokines and growth factors necessary for fibroblast proliferation and neovascularization, leading to effective repair and scar formation. At this stage expression of inhibitory cytokines such as @entity688 may have a role in suppressing the acute inflammatory response and in regulating extracellular matrix metabolism. Fibroblasts in the @entity2318 undergo phenotypic changes expressing smooth muscle cell markers. Our previous review in this journal focused almost exclusively on reduction of the inflammatory injury. The current update is prompted by the potential therapeutic opportunity that the open vessel offers. By promoting more effective tissue repair, it may be possible to reduce the deleterious remodeling, that is the leading cause of @entity712 and @entity204 . Elucidating the complex interactions and regulatory mechanisms responsible for cardiac repair may allow us to design effective inflammation-related interventions for the treatment of @entity583 .

The inflammatory response in XXXX .

@entity1 :: ('9606', 'Species') :: ['patient'] @entity296 :: ('MESH:D009202', 'Disease') :: ['myocardial necrosis', 'Myocardial necrosis'] @entity712 :: ('MESH:D006333', 'Disease') :: ['heart failure'] @entity39 :: ('MESH:D009336', 'Disease') :: ['Necrosis'] @entity63 :: ('MESH:D007511', 'Disease') :: ['ischemic'] @entity2318 :: ('MESH:D002921', 'Disease') :: ['healing scar'] @entity2842 :: ('6347', 'Gene') :: ['Monocyte Chemoattractant Protein (MCP)-1'] @entity1188 :: ('MESH:D007238', 'Disease') :: ['infarcted myocardium'] @entity741 :: ('MESH:D017202', 'Disease') :: ['myocardial ischemia'] @entity583 :: ('MESH:D009203', 'Disease') :: ['myocardial infarction'] @entity687 :: ('3576', 'Gene') :: ['Interleukin (IL)-8'] @entity688 :: ('3586', 'Gene') :: ['IL-10'] @entity204 :: ('MESH:D003643', 'Disease') :: ['death']
@entity583 :: (MESH:D009203,Disease) :: ['myocardial infarction']
