Regulation of CYP7A1 occurs at several levels including synthesis. Bile acids, steroid hormones, inflammatory cytokines, insulin, and growth factors inhibit CYP7A1 transcription through the 5′-upstream region of the promoter.  The average life of this enzyme is between two and three hours.  Activity can be regulated by phosphorylation-dephosphorylation.
CYP7A1 is upregulated by the nuclear receptor LXR (liver X receptor) when cholesterol (to be specific, oxysterol) levels are high.  The effect of this upregulation is to increase the production of bile acids and reduce the level of cholesterol in hepatocytes.
It is downregulated by sterol regulatory element-binding proteins (SREBP) when plasma cholesterol levels are low.
Bile acids provide feedback inhibition of CYP7A1 by at least two different pathways, both involving the farnesoid X receptor, FXR.  In the liver, bile acids bound to FXR induce small heterodimer partner, SHP which binds to LRH-1 and so inhibits the transcription of the enzyme.  In the intestine, bile acids/FXR stimulate production of FGF15/19 (depending on species), which then acts as a hormone in the liver via FGFR4.