Aim To investigate the effect of peroxisome proliferators activated receptorγ (PPARγ) on the calcification of rat aortic vascular smooth muscle cells (VSMC) induced by transforming growth factor-β1 (TGF-β1). Methods Rat aortic vascular smooth muscle cells were cultured in vitro and divided into normal control group and different concentrations of TGF-β1 group (1 μg/L, 2 μg/L, 4 μg/L, 8 μg/L). Then they were divided into normal control group, calcification group (TGF-β1 4 μg/L), rosiglitazone group (RSG, 20 μmol/L), and calcification+rosiglitazone (RSG, 20 μmol/L) group. The effects of agonist RSG on calcification of VSMC, calcium content and alkaline phosphatase (ALP) activity were detected in the cells, alizarin red S staining was used to detect the formation of calcified nodules, and Western blot was used to detect vascular smooth muscle cells marker α-smooth muscle actin (α-SMA), PPARγ, protein expression of osteoblast-like marker Runt-related transcription factor (Runx2). Results Compared with the normal control group, calcium deposition and ALP activity of VSMC treated with TGF-β1 were significantly increased (P<0.05), and the effect was most obvious when TGF-β1 concentration was 4 μg/L. And Runx2 expression of osteoblast-like cell was significantly increased (P<0.05), while α-SMA expression of smooth muscle cell markers was decreased (P<0.05). Whereas calcium sulfate deposition and ALP activity of VSMC were significantly decreased (P<0.05), α-SMA and PPARγ expression was significantly increased after RSG was added(P<0.05), on the contrary, Runx2 expression was significantly inhibited (P<0.05). Conclusion TGF-β1 can induce differentiation and calcification of VSMC into osteoblast-like cells, and TGF-β1-induced calcification of VSMC can be inhibited by PPARγ agonist RSG.