Department of Medicine, Division of Cardiology, Medical University of South Carolina, 30 Courtenay Drive, Charleston, SC 29425, USA.
Division of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.
Cell Signal. 2021 Jan;77:109837. doi: 10.1016/j.cellsig.2020.109837. Epub 2020 Nov 15.
Pathological changes resulting from myocardial infarction (MI) include extracellular matrix alterations of the left ventricle, which can lead to cardiac stiffness and impair systolic and diastolic function. The signals released from necrotic tissue initiate the immune cascade, triggering an extensive inflammatory response followed by reparative fibrosis of the infarct area. Immune cells such as neutrophils, monocytes, macrophages, mast cells, T-cells, and dendritic cells play distinct roles in orchestrating this complex pathological condition, and regulate the balance between pro-fibrotic and anti-fibrotic responses. This review discusses how molecular signals between fibroblasts and immune cells mutually regulate fibrosis post-MI, and outlines the emerging pharmacological targets and therapies for modulating inflammation and cardiac fibrosis associated with MI.
心肌梗死（MI）引起的病理变化包括左心室细胞外基质的改变，这可导致心肌僵硬度增加，并损害心脏的收缩和舒张功能。坏死组织释放的信号启动了免疫级联反应，引发广泛的炎症反应，随后梗死区域发生修复性纤维化。中性粒细胞、单核细胞、巨噬细胞、肥大细胞、T 细胞和树突状细胞等免疫细胞在协调这种复杂的病理状况中发挥着不同的作用，并调节促纤维化和抗纤维化反应之间的平衡。本综述讨论了成纤维细胞和免疫细胞之间的分子信号如何相互调节 MI 后的纤维化，并概述了用于调节 MI 相关炎症和心脏纤维化的新兴药理学靶点和治疗方法。
