CYP7A1 (cytochrome P450 family 7 subfamily A member 1) is a liver-specific microsomal enzyme that catalyzes the first and rate-limiting step in bile acid synthesis by hydroxylating cholesterol at the 7-alpha position to form 7-alpha-hydroxycholesterol 1. As a cytochrome P450 monooxygenase, CYP7A1 uses molecular oxygen to insert one atom into cholesterol substrates while reducing the second into water, with electrons supplied by NADPH via cytochrome P450 reductase 2. Beyond classical bile acid synthesis, CYP7A1 metabolizes oxysterols including 4-beta-hydroxycholesterol and 24-hydroxycholesterol, and oxidizes sterol precursors like 7-dehydrocholesterol 3. CYP7A1 expression is tightly regulated through a gut-liver axis: the intestinal bile acid sensor FXR stimulates FGF15 secretion, which signals to hepatic FGFR4 to suppress CYP7A1 via SHP-mediated mechanisms 1. Additionally, PCSK9 inhibition activates CYP7A1 through PPARα-mediated transcription, promoting cholesterol-to-bile acid conversion 4. CYP7A1 dysregulation contributes to cholesterol gallstone formation and NAFLD pathogenesis, with reduced bile acid synthesis linked to improved lipid metabolism and selective suppression of saturated fatty acid absorption 5. Multiple transcription factors including HNF1α, LXRβ, and MEF2A regulate CYP7A1 expression, with epigenetic modifications influencing hepatic cholesterol homeostasis 67.