Background Dyslipidemia and activation of the intracellular renin-angiotensin system (RAS) are risk factors of the progression of renal tubular interstitial fibrosis (TIF).Epithelial-mesenchymal transition (EMT)plays an important role in the genesis of myofibroblasts during TIF.Our previous in vivo study demonstrated that Rapamycin, an inhibitor of mammalian target of Rapamycin (mTOR), prevented the progression of TIF by overriding lipid accumulation induced by inflammation in apolipoprotein E knockout mice.This study was to investigate potential synergistic effects of dyslipidemia with RAS using human renal epithelial tubular cell line (HK-2) and explore its underlying mechanisms.Methods HK-2 cells were cultured and divided into Control group (treated with serum free medium) and cholesterol loading group (treated with serum free medium plus 30 μg/mL cholesterol and 1 μg/mL 25-hydroxycholesterol).