Immune in myocardial ischemia/reperfusion injury: potential mechanisms and therapeutic strategies

Figures

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  Figure 1. Immune response after myocardial ischemic injury. DAMPs released by necrotic cardiomyocytes bind to PRRs to initiate an immune response. Resident macrophages produce pro-inflammatory cytokines and chemokines, which recruit monocytes and neutrophils to the injured area to remove cellular debris and remodel the extracellular matrix. Dendritic cells present antigens to lymphocytes to activate an adaptive immune response. After entering the repair phase, immune cells transform into a repair phenotype and secrete anti-inflammatory cytokines to mediate the resolution of inflammation. Fibroblasts activate into myofibroblasts, leading to scar formation. DAMPs, damage-associated molecular patterns; PRRs, pattern recognition receptors.

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  Figure 2. Immune cells in three pathological stages after AMI. During the inflammatory phase, immune cells clear dead cells and initiate an inflammatory response. During the proliferative phase, they promote angiogenesis and fiber repair. During the mature phase, immune cells decrease and collagen deposition forms mature scars.

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  Figure 3. Immune cells in cardiac injury and repair. Innate immune cells (neutrophils, macrophages, dendritic cells, innate lymphocytes) and adaptive immune cells (T cells, B cells) in the ischemic heart are involved in cardiac tissue repair and regeneration. ROS, reactive oxygen species; NETs, neutrophil extracellular traps; ECM, extracellular matrix; APC, antigen presenting cell; ILC, innate lymphoid cell; INF-γ, interferon γ; GM-CSF, granulocyte-macrophage colony stimulating factor; TGF-β, transforming growth factor-β; Tregs, regulatory T cells.

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  Figure 4. Macrophages in myocardial infarction. Diverse macrophage phenotypes exist in MI, which secrete multiple cytokines and perform different functions in response to different stimuli. LPS, lipopolysaccharide; GM-CSF, granulocyte-monocyte colony-stimulating factor; IFN, interferon; IL, Interleukin; COX-2, cyclooxygenase 2; TGF-β, transforming growth factor-β; VEGF, vascular endothelial growth factor; CCL17, chemokine (C-C motif) ligand 17; HMOX-1, heme oxygenase-1; CXCL4, C-X-C motif chemokine 4.