Figure 2. The role of the chemokines in cardiac injury.
Both CC and CXC chemokines are induced in the infarcted myocardium. CXC chemokines that contain the ELR motif (such as IL-8) induce neutrophil infiltration and may exert angiogenic effects. In contrast, ELR-negative CXC chemokines (such as IP-10) have angiostatic and antifibrotic properties. Early IP-10 upregulation in the infarcted heart may inhibit granulation tissue formation until the wound is debrided from dead cells and a provisional matrix necessary to support fibroblast and endothelial cell migration is formed. In addition, IP-10 may play a role in recruitment of effector T cells. On the other hand, the CXC chemokine SDF-1 may induce infiltration of CXCR4+ progenitor cells enhancing tissue regeneration and angiogenesis. The best studied CC chemokine is MCP-1, a potent mononuclear cell chemoattractant with angiogenic and pro-fibrotic properties. MCP-1 deficiency is associated with attenuated adverse remodeling at the expense of delayed clearance of the infarct from dead cardiomyocytes. MCP-3, MIP-1α and MIP-1β are also induced in the infarct; however, their role in cardiac injury and repair remains unknown (Symbols: PC, immature progenitor cells; N, neutrophils; Mo, monocytes; L, lymphocytes; EC, endothelial cells; F, fibroblasts).