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. 2025 May 20;17(1):2500099. doi: 10.1080/19490976.2025.2500099

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© 2025 The Author(s). Published with license by Taylor & Francis Group, LLC.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

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Figure 2. — The mechanism of the gut-liver axis: the gut and liver are connected by a complex network of anatomical structures, including the bile ducts, portal vein, and the body’s circulation system. This network facilitates bidirectional communication between the two organs. The liver communicates with the intestine by releasing bile acids and biologically active mediators into the biliary tract and somatic circulation. In the intestine, gut microbiota metabolites are transferred to the liver through the portal vein. The gut microbiota and their metabolites, such as pathogen-associated molecular patterns and endogenous ethanol, SCFA, and BA, can influence the progression of MASLD through a variety of mechanisms. Abbreviations: SCFA: short-chain fatty acids; BA: bile acids; LPS: lipopolysaccharide; AMPK: AMP-activated protein kinase; NF-κB: nuclear factor-κB; IL: interleukin; TNF: tumor necrosis factor; ASBT: apical sodium-bile acid transporter; SHP: small heterodimer partner; FXR: farnesoid X receptor; FGF: fibroblast growth factor.