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. 2025 Oct 9;6:1680031. doi: 10.3389/fragi.2025.1680031

FIGURE 2.

Diagram comparing metabolic pathways in young and aged livers. In young liver, MAOB converts GGOH to GGA, supporting tumor suppression. In aged liver, loss of MAOB reduces GGA levels. CYP3A4 partially compensates but produces insufficient GGA, contributing to a tumor-permissive environment.

Age-dependent shift in hepatic GGA metabolism and its association with tumorigenesis. In young livers (left), monoamine oxidase B (MAOB) is highly expressed and efficiently converts geranylgeraniol (GGOH) to geranylgeranoic acid (GGA), which activates Toll-like receptor 4 signaling and contributes to tumor-suppressive homeostasis. In aged livers (right), the decline or loss of MAOB represents a metabolic turning point, leading to a marked reduction in hepatic GGA levels and the breakdown of tumor-suppressive homeostasis. Although cytochrome P450 3A4 (CYP3A4) partially compensates for this loss, the insufficient GGA levels fail to maintain adequate tumor suppression, resulting in a more tumor-permissive hepatic microenvironment and increased risk of hepatocellular carcinoma.