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Macrophage activation and polarization in post-infarction cardiac remodeling

机译:梗死后心脏重塑中的巨噬细胞活化和极化

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摘要

Adverse cardiac remodeling leads to impaired ventricular function and heart failure, remaining a major cause of mortality and morbidity in patients with acute myocardial infarction. It have been shown that, even if all the recommended therapies for ST-segment elevation myocardial infarction are performed, one third of patients undergoes progressive cardiac remodeling that represents morphological basis for following heart failure. The need to extend our knowledge about factors leading to different clinical scenarios of myocardial infarction and following complications has resulted in a research of immuno-inflammatory pathways and molecular activities as the basis for post-infarction remodeling. Recently, macrophages (cells of the innate immune system) have become a subject of scientific interest under both normal and pathological conditions. Macrophages, besides their role in host protection and tissue homeostasis, play an important role in pathophysiological processes induced by myocardial infarction. In this article we summarize data about the function of monocytes and macrophages plasticity in myocardial infarction and outline potential role of these cells as effective targets to control processes of inflammation, cardiac remodeling and healing following acute coronary event.
机译:不良的心脏重塑导致心室功能受损和心力衰竭,仍然是急性心肌梗死患者死亡和发病的主要原因。已经显示,即使执行了所有建议的ST段抬高型心肌梗死的治疗方法,三分之一的患者也会进行进行性心脏重塑,这代表了心力衰竭的形态学基础。由于需要扩展我们对导致心肌梗塞不同临床情况及随后并发症的因素的认识,因此对免疫炎症途径和分子活性的研究成为了梗死后重塑的基础。近来,巨噬细胞(先天免疫系统的细胞)在正常和病理条件下都已成为科学关注的主题。巨噬细胞除了在宿主保护和组织稳态中发挥作用外,还在心肌梗死诱发的病理生理过程中发挥重要作用。在本文中,我们总结了有关单核细胞和巨噬细胞可塑性在心肌梗死中的功能的数据,并概述了这些细胞作为控制急性冠状动脉事件后炎症,心脏重塑和愈合过程的有效靶标的潜在作用。

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