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The gut–liver axis describes the **bidirectional, functional, and anatomical relationship between the gastrointestinal tract (gut) and the liver**, primarily facilitated through the portal vein, which carries nutrients, microbial metabolites, and antigens from the intestine directly to the liver[1][2][3][5][7]. This axis includes complex interactions between the gut microbiota, the intestinal barrier, immune cells, and liver parenchyma, orchestrating metabolism, immune responses, and homeostasis[1][2][5]. Disruption in this axis—due to altered microbiota, increased permeability (leaky gut), or other stressors—can trigger inflammation, promote the development and progression of liver diseases including non-alcoholic fatty liver disease, cirrhosis, fibrosis, and liver cancer[2][3][4][5][7][8]. While the gut–liver axis is a **biological pathway/system and not a single molecule, protein, or receptor**, it is increasingly targeted by therapies (such as FXR agonists and probiotics) aimed at restoring normal gut-liver crosstalk and preventing or treating liver diseases[3][7]. Thus, the "gut–liver axis" is not itself a molecular target, but rather a physiological concept encompassing multiple molecular, cellular, and systemic components. Caveat: - The gut–liver axis is not a **single molecule, protein, or conventional drug target**, but rather a pathophysiological and anatomical system involving multiple interacting components[2][3][5][7]. - Listing as a drug target is therefore incorrect; instead, it is a **therapeutic axis** frequently targeted by drugs affecting its underlying molecular players.
Modulation of bile acid signaling (especially via FXR agonists); Alteration of gut microbiome composition or function (probiotics, antibiotics); Restoration or protection of the gut barrier; Modification of metabolic byproducts; Suppression of immune/inflammatory mediators
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