Immune regulation of cardiac fibrosis post myocardial infarction.

Immune regulation of cardiac fibrosis post myocardial infarction.
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DOI:
10.1016/j.cellsig.2020.109837
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发表时间:
2021-01
影响因子:
4.8
通讯作者:
DeLeon-Pennell KY
DeLeon-Pennell KY
中科院分区:
生物学2区
文献类型:
--
作者:
Zaidi Y;Aguilar EG;Troncoso M;Ilatovskaya DV;DeLeon-Pennell KY

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心肌梗死(MI)引起的病理改变包括左心室细胞外基质的改变,这可能导致心脏僵硬,损害收缩和舒张期功能。坏死组织释放的信号启动免疫级联反应,引发广泛的炎症反应,随后梗死区出现修复性纤维化。免疫细胞如中性粒细胞、单核细胞、巨噬细胞、肥大细胞、T细胞和树突状细胞在这一复杂的病理状态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。该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心肌梗死后的纤维化,并概述了与心肌梗死相关的炎症和心脏纤维化的新的药理靶点和治疗方法。
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.
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