FGF2 and ischemia: It is suggested that increased extracellular level of hyperhomocysteinaemia in response to cell injury and stress (i.e., ischemia) with Ado [28,29] produces elevated extracellular S-adenosylhomocysteine which in turn, reduces the intracellular mRNA and protein expressions of fibroblast growth factor (FGF2) via G-protein receptor thus, leading to endothelial anti-proliferation (Hcy = 50–100 μM) and anti-survival activity (Hcy > 100 μM) [30,31,32].