Bile acids and their corresponding intestinal epithelial receptors, the farnesoid X receptor (FXR), the G protein-coupled bile acid receptor (TGR5), play crucial roles in the physiological and pathological processes of intestinal epithelial cells. These acids and receptors are involved in the regulation of intestinal absorption, signal transduction, cellular proliferation and repair, cellular senescence, energy metabolism, and the modulation of gut microbiota. A comprehensive literature search was conducted using PubMed, employing keywords such as bile acid, bile acid receptor, FXR (nr1h4), TGR5 (gpbar1), intestinal epithelial cells, proliferation, differentiation, senescence, energy metabolism, gut microbiota, inflammatory bowel disease (IBD), colorectal cancer (CRC), and irritable bowel syndrome (IBS), with a focus on publications available in English. This review examines the diverse effects of bile acid signaling and bile receptor pathways on the proliferation, differentiation, senescence, and energy metabolism of intestinal epithelial cells. Additionally, it explores the interactions between bile acids, their receptors, and the microbiota, as well as the implications of these interactions for host health, particularly in relation to prevalent intestinal diseases. Finally, the review highlights the importance of developing highly specific ligands for FXR and TGR5 receptors in the context of metabolic and intestinal disorders.

Metabolic dysfunction-associated steatohepatitis (MASH) represents a critical hepatic manifestation within the broader spectrum of metabolic syndrome. The pathogenesis of MASH is characterized by disruptions in lipid metabolism, inflammation, and fibrosis. Bile acids and their receptors are integral to the progression of MASH, primarily through their regulatory influence on the metabolic networks of the gut–liver axis. This review offers a comprehensive and systematic examination of the molecular mechanisms underlying bile acid biosynthesis, metabolic dysregulation, and receptor signaling anomalies in MASH. Furthermore, it explores the translational potential of these insights into clinical therapies. Bile acids and their receptors emerge as pivotal therapeutic targets for MASH. Future research should focus on an in-depth analysis of dynamic regulatory mechanisms and the optimization of multi-target combination therapies, thereby paving the way for significant clinical advancements.