Another mechanism that promotes cardiac-resident proliferation is the sensing of tensile forces present in the contracting myocardium, which results in the activation of mitogen-activated protein kinase (MAPK) which particularly signals Mek 1/2 [43], since macrophages increase DNA synthesis when tensile forces are applied in vitro [44,45,46]; the inhibition of Mek 1/2 in in vitro and in vivo after MI reduces cell cycle activity in cardiac macrophages. Here, MAP2K1 is linked to myocardial infarction.