【摘要】 急性心肌梗死(acute myocardial infarction,AMI)造成的心肌细胞死亡引发心脏一系列病理生理反应,其过程涉及促炎反应和细胞外基质降解、抗炎反应和新瘢痕形成。然而,组织损伤引起的强烈炎症反应促使心脏过度纤维化,导致对抗性的心脏重塑,最终发展为心力衰竭等不良心血管事件。了解AMI后的炎症调控机制有助于防治不良预后。本综述介绍了AMI后心脏修复中的关键炎症因子白细胞介素、基质金属蛋白酶、活性氧等,通过发挥自身的促炎和抗炎作用影响AMI后梗死面积以及左室功能,从而调控AMI后的心脏修复,为临床上改善AMI患者预后提供依据和策略。更多还原

【Abstract】 Acute myocardial infarction( AMI) induced cardiomyocyte death causes a series of pathophysiological responses of the heart. The process involves pro-inflammatory reaction and extracellular matrix degradation,and anti-inflammatory reaction and new scars formation. However,the redundancy of inflammatory reaction caused by tissue injury would lead to excessive cardiac fibrosis and antagonistic cardiac remodeling,eventually developing into adverse cardiovascular events such as heart failure. It is helpful to prevent and treat the adverse prognosis after AMI as far as understanding the inflammatory regulation mechanism. This review introduces the key inflammatory factors involved in cardiac repair after AMI,especially interleukin,matrix metalloproteinase and reactive oxygen species,influence the infarct area and left ventricular function after AMI through pro-and anti-inflammatory effects of themselves. These factors regulate cardiac repair after AMI,and provide references and strategies for clinically improving the prognosis of patients with AMI.更多还原