Table 2:

The cellular events associated with inflammatory phase of the remodeling of IZ following MI.

Cells	Inflammatory Response	References
Cardiomyocytes	Necrotic and surviving cardiomyocytes stimulates inflammatory responses, DAMP activation, and ROS generation	[11]
Endothelial cells	Promotes the infiltration of immune cells and stem cells to IZ	[17]
Neutrophils	DAMP signaling, secretion of inflammatory mediators, and ECM degradation	[11]
Monocyte subpopulations	Early phase pro-inflammatory Ly6Chi monocytes activates via MCP-1 receptor to trigger phagocytosis, ECM degradation and inflammation, where the late phase anti-inflammatory Ly-6Clo monocytes acts via CX3CR1to facilitate myofibroblast accumulation, angiogenesis and ECM deposition	[18]
Lymphocytes	Subpopulations of CD4+/CD8+ T-cells, Foxp3+ regulatory cells (Tregs), invariant natural killer (iNK) T-cells, and γδT-cells aids in wound healing	[11]
Fibroblasts	DAMP signaling and cytokine secretion, ECM synthesis and fibrosis	[19]
Mast cells	Perivascular mast cells release TNF, histamine and tryptase to trigger inflammation	[11]
Macrophages	Two subsets: pro-inflammatory M1 and anti-inflammatory M2 populations	[20]
Dendritic cells	Mo/Mϕ, CD11c+ dendritic cells activate scarring and angiogenesis	[21]