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The Transforming Growth Factor-beta (TGF-β) pathway regulates relevant processes during liver development and homeostasis and becomes a relevant factor involved in liver pathologies. Different members of the family of NADPH Oxidases (NOXs) are targets of the TGF-β pathway and mediate some of its effects in the liver. In this chapter, we focus on the complex role of the axis TGF-β/NOXs regulating the behavior of different liver cells, such as hepatocytes, hepatic stellate cells or macrophages, and how this influences the initiation and/or progression of liver fibrotic diseases and cancer. Different NOXs (NOX1, NOX2, NOX4) appear to be involved in the activation of hepatic stellate cells (HSC) to myofibroblasts, contributing to liver fibrosis. Indeed, inhibiting NOX1/NOX4 is being considered a therapeutic option in fibrotic processes. More complex is the situation in cancer, where data strongly support a transformation role for some members of the family, such as NOX1 and NOX2, but the case of NOX4 is more complex since it mediates TGF-β-induced tumor suppressor but also pro-migratory signals. We will discuss how important is to better understand this complexity for considering TGF-β and/or NOX inhibitors in liver cancer therapies.

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The TGF-β/NADPH Oxidases Axis in the Regulation of Liver Fibrosis and Cancer

  • 章节

  • 发表日期：

    2026年

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  • Josep Amengual,
  • Rut Espinosa-Sotelo,
  • Ana Cantos-Cortés,
  • Gemma Gonfaus-Ortiz,
  • Ania Alay,
  • Victoria Campuzano,
  • Gustavo Egea,
  • Esther Bertran,
  • Isabel Fabregat

摘要

The Transforming Growth Factor-beta (TGF-β) pathway regulates relevant processes during liver development and homeostasis and becomes a relevant factor involved in liver pathologies. Different members of the family of NADPH Oxidases (NOXs) are targets of the TGF-β pathway and mediate some of its effects in the liver. In this chapter, we focus on the complex role of the axis TGF-β/NOXs regulating the behavior of different liver cells, such as hepatocytes, hepatic stellate cells or macrophages, and how this influences the initiation and/or progression of liver fibrotic diseases and cancer. Different NOXs (NOX1, NOX2, NOX4) appear to be involved in the activation of hepatic stellate cells (HSC) to myofibroblasts, contributing to liver fibrosis. Indeed, inhibiting NOX1/NOX4 is being considered a therapeutic option in fibrotic processes. More complex is the situation in cancer, where data strongly support a transformation role for some members of the family, such as NOX1 and NOX2, but the case of NOX4 is more complex since it mediates TGF-β-induced tumor suppressor but also pro-migratory signals. We will discuss how important is to better understand this complexity for considering TGF-β and/or NOX inhibitors in liver cancer therapies.