【Abstract】 Objective To evaluate the expression of PiT-1 in hyperphosphatemia induced thoracic aorta calcification and its underlying mechanism in chronic renal failure (CRF) rats. Methods A total of 36 male Wistar rats were subjected to nephrectomy of 5/6 kidneys (n=27) or sham operation group (n=9). After the operation, rats were fed with regular diet for 4 weeks, and then with high phosphorous diet for 10 weeks. From beginning of the high phosphorous diet, rats were divided into 3 groups: (a) Model group (nephrectomy + high phosphorous diet, n=9), (b) phosphonoformic acid (PFA) treated group (nephrectomy + high phosphorous diet + intraperitoneal PFA 0.15 g/kg/every other day, n=7) (c) Control group (nephrectomy + high phosphorous diet + intraperitoneal normal saline infection/every other day, n=6). At the end of high phosphorous diet, rats were sacrificed. Serum creatinine, Ca, inorganic phosphorous and 1,25(OH)2D3 were measured. The upper part of thoracic aorta was used for calcium content assay, the middle part was stored at -800C for the measurement of Pit-1 and Cbfα-1 and their mRNAs by western blot and quantitative real-time PCR, and the paraffin slides of the lower part were treated with von Kossa staining. Results There were no significant differences in serum creatinine, Ca, inorganic phosphorous and 1,25(OH)2D3 among CRF rats at the beginning and end of high phosphorous diet. In PFA treated group, Pit-1 and its mRNA in aorta decreased, as compared with those in model and control group (P<0.001), and Cbfα-1 and its mRNA also decreased (P<0.001), in accompanying with the less degree of aorta calcification. Conclusions In rats with CRF and hyperphosphatemia, PiT-1 in thoracic aorta mediated the transportation of phosphate, induced the over-expression of Cbfα-1, and promoted vascular calcification.