Abstract: The aim of this study was to study the changes in the expression of transforming growth factor β1 (TGFβ1), the TGFβ1 receptor (TβRI), Smad7, and histone deacetylase 1 (HDAC1) in mice with aristolochic acid nephropathy (AAN), and analyze the relationship between HDAC1 and Smad7. RTPCR was applied to detect the mRNA levels of TGFβ1, Smad7 and HDAC1 in kidneys. The TGFβ concentrations were determined by ELISA. HADC1 and Smad7 proteins were localized and detected by immunohistochemistry method. The tissue section technique was used to observe the histopathologic changes, such as kidney damage and renal tubules interstitial fibrosis degree. Results were as follows: In mice with induced AAN, the mRNA levels for TGFβ1and HDAC1 were increased with treatment time. The mRNA levels for TGFβ1 were higher than that of their control (normal mice without treatment) (P<0.05). Starting from 28 day, mRNA of HDAC1 became significantly higher than the level of the control (P<0.01). The levels of Smad7 protein and its mRNA were decreased with time, and lower than that of control. HDAC1 protein expression was increased with time post treatment. Compared with the control group, HDAC1 positive stains were mainly distributed in the epithelial and stromal cell nucleus. Histopathologic changes of kidney showed acute tubular interstitial damage, such as turbidity, swollen, degeneration and fall off of renal tubular. With extension of treatment time, renal tubular damage was aggravated progressively. During the development of AAN in mice, Smad7 can cause renal tubular damage, impare renal tubular renewable repair ability, restrain Smad7 mRNA expression. The weak expression of Smad7 in renal tissues can promote TGFβ1 signal transduction, help the fibre formation and maintain the proliferation condition. One of the mechanism happened is about HDACl, which mRNA and protein high expressions plays an important role in the development aristolochinc acid nephropathy, may be a new potential target.