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<p>Dysfunction of the gut–liver axis is a&#xa0;key pathomechanism for progression of liver cirrhosis and the development of life-threatening complications. This review summarizes the current state of knowledge on the gut–liver axis and highlights its clinical relevance. Disease progression is driven by a&#xa0;vicious cycle of portal hypertension (PHT) and systemic inflammation (SI), in which cirrhosis-associated dysbiosis and impaired intestinal barrier function enable pathological bacterial translocation, which in turn perpetuates SI as the main driver and aggravates PHT. This mechanism is largely responsible for the development of complications such as spontaneous infections, hepatic encephalopathy, and acute-on-chronic liver failure (ACLF). A&#xa0;deeper understanding of these interactions not only underpins the rational use of established therapies but also opens up new perspectives for diagnostic and therapeutic strategies aiming to restore gut–liver homeostasis.</p>

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Die Darm-Leber-Achse bei Leberzirrhose

  • 期刊论文

  • 发表日期：

    2026年1月21日

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  • Tony Bruns,
  • Jonel Trebicka

摘要

Dysfunction of the gut–liver axis is a key pathomechanism for progression of liver cirrhosis and the development of life-threatening complications. This review summarizes the current state of knowledge on the gut–liver axis and highlights its clinical relevance. Disease progression is driven by a vicious cycle of portal hypertension (PHT) and systemic inflammation (SI), in which cirrhosis-associated dysbiosis and impaired intestinal barrier function enable pathological bacterial translocation, which in turn perpetuates SI as the main driver and aggravates PHT. This mechanism is largely responsible for the development of complications such as spontaneous infections, hepatic encephalopathy, and acute-on-chronic liver failure (ACLF). A deeper understanding of these interactions not only underpins the rational use of established therapies but also opens up new perspectives for diagnostic and therapeutic strategies aiming to restore gut–liver homeostasis.