<p>In recent years, growing evidence has underscored the pivotal roles of gut microbiota dysbiosis and disrupted amino acid metabolism in the development of metabolic dysfunction-associated fatty liver disease-related hepatocellular carcinoma (MAFLD-HCC). These factors not only drive HCC progression but also have a profound impact on the tumor immune microenvironment (TIME). Despite substantial advances, critical questions remain regarding how modulation of gut microbiota and amino acid metabolism can influence tumor immunity. This review examines the intricate interactions among intestinal microbiota, amino acid metabolism, and the TIME, emphasizing their contributions to the progression from MAFLD to HCC. In addition, we discuss potential therapeutic approaches, including dietary interventions, probiotic supplementation, and metabolic modulators that may improve clinical outcomes in MAFLD-HCC. By integrating these perspectives, this review aims to provide novel insights for the development of targeted strategies to enhance prognosis in affected patients.</p>

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Mechanistic roles and intervention strategies involving gut microbiota, amino acid metabolism, and the tumor immune microenvironment in MAFLD-HCC progression

  • Ziwei Guo,
  • Ziang Yao,
  • Xiaohan Chen,
  • Dongjie Wu,
  • Yaqi Ouyang,
  • Yaocun Shen,
  • Yi Wang,
  • Houyan Zhang,
  • Yanping Lu,
  • Wenliang Lv

摘要

In recent years, growing evidence has underscored the pivotal roles of gut microbiota dysbiosis and disrupted amino acid metabolism in the development of metabolic dysfunction-associated fatty liver disease-related hepatocellular carcinoma (MAFLD-HCC). These factors not only drive HCC progression but also have a profound impact on the tumor immune microenvironment (TIME). Despite substantial advances, critical questions remain regarding how modulation of gut microbiota and amino acid metabolism can influence tumor immunity. This review examines the intricate interactions among intestinal microbiota, amino acid metabolism, and the TIME, emphasizing their contributions to the progression from MAFLD to HCC. In addition, we discuss potential therapeutic approaches, including dietary interventions, probiotic supplementation, and metabolic modulators that may improve clinical outcomes in MAFLD-HCC. By integrating these perspectives, this review aims to provide novel insights for the development of targeted strategies to enhance prognosis in affected patients.