TGFB1 and infarction: Reduction in:-Inflammation, fibrosis, and oxidative stress in the kidneys [112];-Levels of Gal-3, TGF-β, IL-1β, and CD80-positive pro-inflammatory M1 macrophages [124,125];-Apoptosis of myocytes in the peri-infarction zone by 40%–50% [126];-Mesangial fibrosis and glomerulonephritis [130];-Concentration of ROIs and CRP [132];-Oxidative stress signaling pathways, leading to an increase in bioavailable nitric oxide, inflammation, cell proliferation, and the rate of fibrosis [135].Increase in:-CD163-positive anti-inflammatory M2 macrophages in infarction [124,125].