Bile acids (BAs) are amphipathic molecules synthesized from cholesterol in hepatocytes and serve as essential regulators of lipid digestion, nutrient absorption, and cholesterol homeostasis. Beyond their classical detergent role in bile, BAs function as signaling molecules that modulate gene expression and cellular processes through nuclear and membrane-bound receptors, including the farnesoid X receptor (FXR) and Takeda G-protein receptor 5 (TGR5). Dysregulation of BA synthesis, transport, or signaling contributes to the pathogenesis of a wide range of hepatic and biliary disorders, including cholestatic liver diseases, non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), hepatocellular carcinoma (HCC), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC). Advances in understanding BA-mediated molecular pathways have revealed novel therapeutic targets, such as FXR/TGR5 agonists, bile acid sequestrants, and ursodeoxycholic acid (UDCA), which offer clinical benefits in the management of these disorders. This review comprehensively discusses the physiological functions of BAs, their signaling mechanisms, dysregulation in hepatic and biliary diseases, and current and emerging therapeutic strategies, highlighting their translational potential in personalized medicine.