Figure 6
Schematic depiction of SP and the NK-1R regulation of cardiac MCs and fibrosis. SP activation of the NK-1R causes an increase in cardiac MC density in the heart by increasing SCF production by endothelial cells, cardiomyocytes, and fibroblasts. While MCs are known to cause fibrosis, the NK-1R is not required for the activation of cardiac MCs. SP also acts to increase the number of myofibroblasts, however, it is not clear whether this is a direct effect on myofibroblast proliferation or a by-product of increasing the number of mature MCs that then act to increase myofibroblast numbers.
