炎症
纤维化
免疫系统
心脏纤维化
免疫学
渗透(HVAC)
再生(生物学)
医学
病理
生物
巨噬细胞
伤口愈合
细胞生物学
体外
物理
热力学
生物化学
作者
William P. Lafuse,Daniel J. Wozniak,Murugesan V. S. Rajaram
出处
期刊:Cells
[Multidisciplinary Digital Publishing Institute]
日期:2020-12-31
卷期号:10 (1): 51-51
被引量:187
标识
DOI:10.3390/cells10010051
摘要
The immune system plays a pivotal role in the initiation, development and resolution of inflammation following insult or damage to organs. The heart is a vital organ which supplies nutrients and oxygen to all parts of the body. Heart failure (HF) has been conventionally described as a disease associated with cardiac tissue damage caused by systemic inflammation, arrhythmia and conduction defects. Cardiac inflammation and subsequent tissue damage is orchestrated by the infiltration and activation of various immune cells including neutrophils, monocytes, macrophages, eosinophils, mast cells, natural killer cells, and T and B cells into the myocardium. After tissue injury, monocytes and tissue-resident macrophages undergo marked phenotypic and functional changes, and function as key regulators of tissue repair, regeneration and fibrosis. Disturbance in resident macrophage functions such as uncontrolled production of inflammatory cytokines, growth factors and inefficient generation of an anti-inflammatory response or unsuccessful communication between macrophages and epithelial and endothelial cells and fibroblasts can lead to aberrant repair, persistent injury, and HF. Therefore, in this review, we discuss the role of cardiac macrophages on cardiac inflammation, tissue repair, regeneration and fibrosis.
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