TGFB1 and Hyperglycemia: These complex and progressive pathologic changes are mainly induced by (a) hyperglycemia and enhanced formation of advanced glycation end products (AGE); (b) increased activity of angiotensin II (Ang II) within the renin-angiotensin system; (c) excessive TGFβ-signaling; (d) chronic inflammation associated to enhanced recruitment of leukocytes and release of proinflammatory cytokines, chemokines and growth factors [6, 7].