Figure 8.

Proposed schematic representation illustrates the involvement of nicorandil in macrophage‐ and myofibroblast‐related cardiac fibrosis in post‐infarcted rats. After MI, during the early stage, it is characterized by inflammatory M1 phenotype macrophages, however, at a late stage, M2 phenotype would become dominant. M1 and M2 phenotype macrophages can be converted into each other. IL‐10 activity in M2 macrophages inhibits myofibroblast differentiation, which antagonizes extracellular matrix production. Nicorandil administration exhibits potent anti‐fibrotic activity by suppressing collagen synthesis via increasing the activation of M2 macrophages and inhibiting myofibroblast differentiation.