AGEs also increase the expression of KCa3.1 channels in a RAGE-dependent manner by activation of ERK1/2, p38-MAPK, and PI3K/Akt signalling, thereby promoting the proliferation of cardiac fibroblasts and ECM (114), which is another mechanism of deposition of ECM components that correlates to myocardial fibrosis. Here, AGER is linked to Myocardial fibrosis.