Cholesterol and the gut-liver axis: unraveling their role in the onset and progression of metabolic-associated steatotic liver disease
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Le résumé fourni par la source
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of chronic liver disease worldwide. Its prevalence is increasing due to its close relationship with obesity, insulin resistance, and other metabolic disorders. In this context, the gut-liver axis has been identified as a fundamental regulator in the progression of MASLD, integrating metabolic, immunological, and inflammatory signals that influence hepatic homeostasis. This article reviews the interconnection between the intestine and the liver in the onset and progression of MASLD, highlighting the roles of cholesterol and its metabolism, intestinal barrier permeability, microbiota, and hepatic signaling pathways. We analyze how intestinal dysbiosis and alterations in the enterohepatic circulation of bile acids affect cholesterol absorption and metabolism. Furthermore, we address the influence of endotoxin translocation, activation of the innate immune system, and the interaction of key transcription factors on disease progression from steatosis to advanced fibrosis and hepatocellular carcinoma (HCC). Finally, therapeutic strategies, including pharmacological, dietary, and immunomodulation-based approaches, are discussed to regulate cholesterol metabolism, modulate the intestinal microbiota, and restore gut-liver axis homeostasis. Integrating this knowledge could open new perspectives for treating and preventing MASLD, addressing the disease from a broader and multidisciplinary viewpoint.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Cholesterol and the gut-liver axis: unraveling their role in the onset and progression of metabolic-associated steatotic liver disease
- Date Crossref
- 05/08/2025
- Éditeur
- Open Exploration Publishing
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
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