In our previous study, we found that PFN-1 plays an important role in AGEs-induced endothelial abnormalities via promoting cytoskeleton rearrangement and redistribution [28] and silencing the expression of PFN-1 attenuated AGEs-induced myocardium injury including cardiac hypertrophy and fibrosis in vivo [29]. This evidence concerns the gene PFN1 and cardiac hypertrophy.