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The **bile acids synthesis pathway** describes the multi-step biochemical process primarily occurring in the liver in which cholesterol is converted into bile acids. This is achieved via two routes: the classic (neutral) pathway, initiated by cholesterol 7α-hydroxylase (CYP7A1), and the alternative (acidic) pathway, initiated by sterol 27-hydroxylase (CYP27A1). Bile acids are further conjugated (e.g., to glycine or taurine), secreted into bile, and play crucial roles in dietary fat absorption, cholesterol homeostasis, and signaling through nuclear and membrane receptors such as FXR and TGR5. Disturbances in this pathway are implicated in diverse metabolic and liver diseases. While individual enzymes and receptors within this pathway are validated drug targets, the pathway as a whole is not a single molecular target, but an essential metabolic network central to hepatic and systemic physiology[1][3][5][7][6].
Inhibition or activation of individual pathway enzymes (e.g., CYP7A1) Modulation of bile acid receptors (e.g., FXR, TGR5) affecting synthesis and enterohepatic circulation Bile acid sequestration/interruption of enterohepatic recirculation
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