Abstract
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.
Highlights
Macrophages are the central regulator of immune systems, able to activate and proliferate lymphocytes to generate innate and adaptive immune response [1]
We demonstrated that the M. avium infection in aged mice enhances the recruitment of CD45+ leukocytes into the heart and increased expression of inflammatory cytokines, which results in the induction of cardiac fibrosis and cardiac hypertrophy [59]
pattern recognition receptors (PRRs) are divided into two groups based on their subcellular localization: toll-like receptors (TLRs) and C-type lectin receptors are present on plasma membranes or endosomes and the second class of PRRs, including retinoic acid inducible gene –I- like receptors (RLRs), nucleotide binding and oligomerization domain (NOD)-like receptors and absentin-melanoma-2 (AIM2) receptors, are localized in intracellular compartments [117,118]
Summary
Macrophages are the central regulator of immune systems, able to activate and proliferate lymphocytes to generate innate and adaptive immune response [1]. The immune system provides a protective inflammatory response necessary for host defense from infections and plays a critical role in resolving local damage caused by sterile inflammation in the heart. Cells 2021, 10, 51 role in resolving local damage caused by sterile inflammation in the heart. Macrophages are the central regulator of immune systems [1], and the primary immune cells that reside in the heart tissue during steady state [5,6]. Cardiac immune cells are activated by sterile either inflamsterile inflammation tissue injury or infection. Regulatory T cells are found sporadically in cardiac tissue
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